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1. George TI, Wrede JE, Bangs CD, Cherry AM, Warnke RA, Arber DA: Low-grade B-Cell lymphomas with plasmacytic differentiation lack PAX5 gene rearrangements. J Mol Diagn; 2005 Aug;7(3):346-51
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  • [Title] Low-grade B-Cell lymphomas with plasmacytic differentiation lack PAX5 gene rearrangements.
  • The chromosomal translocation t(9;14)(p13;q32) has been reported in association with lymphoplasmacytic lymphoma (LPL).
  • Although this translocation involving the paired homeobox-5 (PAX5) gene at chromosome band 9p13 and the immunoglobulin heavy chain (IgH) gene at 14q32 has been described in approximately 50% of LPL cases, the actual number of cases studied is quite small.
  • Many of the initial cases associated with t(9;14)(p13;q32) were actually low-grade B-cell lymphomas with plasmacytic differentiation other than LPL.
  • Thus, we analyzed a series of low-grade B-cell lymphomas for PAX5 gene rearrangements.
  • We searched records from the Department of Pathology, Stanford University Medical Center for low-grade B-cell lymphomas, with an emphasis on plasmacytic differentiation, that had available paraffin blocks or frozen tissue.
  • We identified 37 cases, including 13 LPL, 18 marginal zone lymphomas (nodal, extranodal, splenic, and alpha-heavy chain disease), and 6 small lymphocytic lymphomas.
  • All cases failed to demonstrate a PAX5 translocation, indicating that t(9;14)(p13;q32) and other PAX5 translocations are uncommon events in low-grade B-cell lymphomas with plasmacytic differentiation.

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  • (PMID = 16049306.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA034233; United States / NCI NIH HHS / CA / CA34233
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / DNA Probes; 0 / DNA-Binding Proteins; 0 / PAX5 protein, human; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1867539
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2. Jiang X, Ren YP, Lv ZR: Ouabain induces cardiac remodeling in rats independent of blood pressure. Acta Pharmacol Sin; 2007 Mar;28(3):344-52
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  • After 4 and 6 weeks, echocardiography were performed, hemodynamic parameters were measured by invasive cardiac catheterization, changes in cardiac ultrastructure were analyzed using transmission electron microscopy, the collagen fraction of the left ventricle was assessed with Picrosirius red stain, and RT-PCR was applied to evaluate the mRNA level of myosin heavy chain-alpha and -beta in the left ventricle.
  • Moreover, the cardiac MHC-beta mRNA was upregulated by ouabain treatment, whereas MHC-alpha mRNA was downregulated.
  • [MeSH-minor] Animals. Echocardiography. Glyceraldehyde-3-Phosphate Dehydrogenases / biosynthesis. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Male. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17302996.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 5ACL011P69 / Ouabain; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.6.4.1 / Myosin Heavy Chains
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3. Sekine H, Shimizu T, Yang J, Kobayashi E, Okano T: Pulsatile myocardial tubes fabricated with cell sheet engineering. Circulation; 2006 Jul 4;114(1 Suppl):I87-93
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  • METHODS AND RESULTS: Neonatal rat cardiomyocyte sheets were sequentially wrapped around a resected adult rat thoracic aorta and transplanted in place of the abdominal aorta of athymic rats (n=17).
  • Finally, when myocardial tubes used for aortic replacement were compared with grafts implanted in the abdominal cavity (n=7), we observed significantly increased tissue thickness, as well as expression of brain natriuretic peptide, myosin heavy chain-alpha, and myosin heavy chain-beta.
  • [MeSH-major] Aorta, Abdominal / surgery. Myocardial Contraction. Myocardium / cytology. Myocytes, Cardiac / transplantation. Tissue Engineering / methods
  • [MeSH-minor] Animals. Animals, Newborn. Aorta, Thoracic / transplantation. Cell Culture Techniques / instrumentation. Cells, Cultured / transplantation. Electrocardiography. Gene Expression Profiling. Microsurgery. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Natriuretic Peptide, Brain / biosynthesis. Natriuretic Peptide, Brain / genetics. Organ Culture Techniques. Rats. Rats, Nude. Rats, Wistar. Temperature

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  • (PMID = 16820651.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bmyo protein, rat; 0 / natriuretic peptide precursor type B, rat; 114471-18-0 / Natriuretic Peptide, Brain; EC 3.6.4.1 / Myosin Heavy Chains
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4. Vaiphei K, Kumari N, Sinha SK, Dutta U, Nagi B, Joshi K, Singh K: Roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease. World J Gastroenterol; 2006 Jun 14;12(22):3602-8
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  • [Title] Roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease.
  • AIM: To evaluate roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease (IPSID) and to study profiles of kappa (kappa) and lambda (lambda) light chains and IgA heavy chain.
  • METHODS: The study consisted of 11 cases of IPSID and similar number of controls which included 11 of normal intestinal mucosa and 11 of high grade B cell lymphoma of ileum.
  • The parameters analyzed included clinical profiles, biochemical and other laboratory investigations, radiologic and histological findings including immunohistochemistry.
  • RESULTS: All IPSID cases had demonstrable serum IgA heavy chain and heavy mucosal plasma cell infiltration.
  • According to Galian's histological staging, there were 4 patients with stage A and 7 with stage B. kappa and lambda light chains were over-expressed in 7 patients; 1 stage A patient had H pylori-positive active gastritis and eradication of H pylori led to disease remission.
  • Syndecan-1, kappa and lambda light chains and IgA heavy chain showed inverse relationship with bcl6 and p53.
  • CHOP regime was added in 5 patients who developed frank lymphoma.
  • Three died of the disease due to extensive organ infiltration.
  • CONCLUSION: Certain immunomarkers like syndecan-1, kappa and lambda light chains and IgA heavy chain could be of much help in identifying early stage IPSID.
  • Stage B IPSID showed higher expression for bcl6 and p53 than stage A IPSID. bcl6 and p53 expressions correlated with a more advanced disease stage and aggressive tumour behavior.
  • [MeSH-major] DNA-Binding Proteins / genetics. Immunoproliferative Small Intestinal Disease / diagnosis. Immunoproliferative Small Intestinal Disease / genetics. Membrane Glycoproteins / genetics. Proteoglycans / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Case-Control Studies. Disease Progression. Doxycycline / therapeutic use. Endoscopy, Gastrointestinal. Female. Gene Expression Regulation. Helicobacter pylori. Humans. Immunoglobulin alpha-Chains / blood. Immunoglobulin alpha-Chains / genetics. Immunoglobulin kappa-Chains / analysis. Immunoglobulin kappa-Chains / genetics. Immunoglobulin lambda-Chains / analysis. Immunoglobulin lambda-Chains / genetics. Immunohistochemistry. Intestinal Mucosa / chemistry. Intestinal Mucosa / microbiology. Intestinal Mucosa / pathology. Intestine, Small / chemistry. Intestine, Small / microbiology. Intestine, Small / pathology. Male. Middle Aged. Prognosis. Syndecan-1. Syndecans

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  • (PMID = 16773719.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / Immunoglobulin alpha-Chains; 0 / Immunoglobulin kappa-Chains; 0 / Immunoglobulin lambda-Chains; 0 / Membrane Glycoproteins; 0 / Proteoglycans; 0 / SDC1 protein, human; 0 / Syndecan-1; 0 / Syndecans; 0 / Tumor Suppressor Protein p53; N12000U13O / Doxycycline
  • [Other-IDs] NLM/ PMC4087578
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5. Dutta U, Udawat H, Noor MT, Sidhu GS, Kochhar R, Vaiphei K, Singh K: Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori. J Gastrointest Cancer; 2010 Sep;41(3):212-5
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  • [Title] Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori.
  • A 20-year-old male presented with low-grade fever, abdominal pain, anorexia, and weight loss of 4-month duration.
  • Contrast-enhanced computed tomography of the abdomen revealed extensive proximal small-bowel thickening with mesenteric lymphadenopathy.
  • Upper gastrointestinal endoscopy and enteroscopy revealed thickening of folds with multiple small superficial ulceration involving antrum, duodenum, and jejunum.
  • The duodenal and jejunal biopsy was suggestive of immunoproliferative small intestinal disease, stage 0 (Salem) or stage A (Galian).
  • He underwent H. pylori eradication following which he had significant clinical improvement; repeat evaluation at 6 months showed dramatic improvement in his clinical, radiological, and histological parameters.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Helicobacter Infections / complications. Immunoproliferative Small Intestinal Disease / drug therapy. Immunoproliferative Small Intestinal Disease / microbiology

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  • (PMID = 20300878.001).
  • [ISSN] 1941-6636
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Bacterial Agents; 0 / Organometallic Compounds; 033KF7V46H / Tinidazole; 0K5C5T2QPG / Lansoprazole; 804826J2HU / Amoxicillin; H1250JIK0A / Clarithromycin; HS813P8QPX / bismuth tripotassium dicitrate; KG60484QX9 / Omeprazole; N12000U13O / Doxycycline
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6. Zheng H, Li M, Ren W, Zeng L, Liu HD, Hu D, Deng X, Tang M, Shi Y, Gong J, Cao Y: Expression and secretion of immunoglobulin alpha heavy chain with diverse VDJ recombinations by human epithelial cancer cells. Mol Immunol; 2007 Mar;44(9):2221-7
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  • [Title] Expression and secretion of immunoglobulin alpha heavy chain with diverse VDJ recombinations by human epithelial cancer cells.
  • Recently, we found the expression of Ig alpha heavy chain in human epithelial cancer cells unexpectedly.
  • Further, the configuration of the Ig heavy chain genomic locus was analyzed in human cancer cells.
  • These provide further proofs for Ig alpha expression.
  • In addition, we found that human cancer cells not only express the protein of Ig alpha chain, but also secrete the protein in secretory IgA (SIgA) pattern.
  • Since IgA is the key immunoglobulin which contributes to local immunity of mucous membrane, the aberrant expression of Ig alpha heavy chain might increase our further comprehension to development and immunity of cancers.
  • [MeSH-major] Epithelial Cells / immunology. Epithelial Cells / pathology. Immunoglobulin A, Secretory / genetics. Immunoglobulin alpha-Chains / genetics. Neoplasms / immunology. Recombination, Genetic. VDJ Exons / genetics

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  • (PMID = 17174398.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Immunoglobulin A, Secretory; 0 / Immunoglobulin alpha-Chains; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RAG2 protein, human; 0 / RNA, Messenger; 128559-51-3 / RAG-1 protein; EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase
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7. Huang YC, Khait L, Birla RK: Modulating the functional performance of bioengineered heart muscle using growth factor stimulation. Ann Biomed Eng; 2008 Aug;36(8):1372-82
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  • Also, at 25 ng/mL, myosin heavy chain alpha and SERCA2 expression increased by 1.3 +/- 0.188 and 1.1 +/- 0.04 fold, respectively.

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  • (PMID = 18500554.001).
  • [ISSN] 1573-9686
  • [Journal-full-title] Annals of biomedical engineering
  • [ISO-abbreviation] Ann Biomed Eng
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins
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8. Dillmann W: Cardiac hypertrophy and thyroid hormone signaling. Heart Fail Rev; 2010 Mar;15(2):125-32
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  • These multiple thyroid hormone effects are largely mediated by the action of nuclear based thyroid hormone receptors (TR) the thyroid hormone receptor alpha and beta.
  • Related to myofibrillar proteins, myosin heavy chain alpha is increased by T3 and MHC beta is decreased.
  • [MeSH-minor] Animals. Humans. Myosin Heavy Chains / metabolism. Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism

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  • (PMID = 19125327.001).
  • [ISSN] 1573-7322
  • [Journal-full-title] Heart failure reviews
  • [ISO-abbreviation] Heart Fail Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Thyroid Hormone; 0 / Thyroid Hormones; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; EC 3.6.4.1 / Myosin Heavy Chains; SY7Q814VUP / Calcium
  • [Number-of-references] 60
  • [Other-IDs] NLM/ PMC2820695
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9. Mielcarek-Kuchta D, Olofsson J, Golusinski W: Laminin expression in advanced laryngeal squamous cell carcinoma does not correlate to neck metastases. Eur Arch Otorhinolaryngol; 2008 Oct;265(10):1257-61
Genetic Alliance. consumer health - Carcinoma, Squamous Cell.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Laminins are a family of glycoproteins that consist of one heavy alpha chain and two light beta and gamma chains.
  • The study was carried out on 70 patients with squamous cell carcinoma of the larynx treated at the ENT Department University of Medical Sciences in Poznań.
  • The clinical data consisted of sex, age, stage of the tumor, and histological and immunohistochemical studies.
  • The patients with advanced clinical disease dominated in our material.

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  • (PMID = 18516614.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Laminin
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10. Zhou H, Hickford JG, Fang Q: Identification of allelic polymorphism in the caprine IGHA gene. Dev Comp Immunol; 2006;30(9):741-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Variation in the immunoglobulin heavy alpha chain (IGHA) constant region has been reported in a number of species.
  • The variation reported here may affect the structure of the hinge and hence the function of IgA.
  • [MeSH-major] Goats / genetics. Goats / immunology. Immunoglobulin alpha-Chains / genetics
  • [MeSH-minor] Alleles. Amino Acid Sequence. Animals. Base Sequence. DNA / chemistry. DNA / genetics. Hinge Exons. Molecular Sequence Data. Polymerase Chain Reaction / veterinary. Polymorphism, Single-Stranded Conformational. Sequence Alignment

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  • (PMID = 16343618.001).
  • [ISSN] 0145-305X
  • [Journal-full-title] Developmental and comparative immunology
  • [ISO-abbreviation] Dev. Comp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin alpha-Chains; 9007-49-2 / DNA
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11. Ben Ammar A, Cheikh I, Jouini M, Belkahla N, Fadhel SF, Hager O, Maamouri N, Chaabouni H, Ben Safta Z, Haouet S: [Alpha heavy chain disease. A Tunisian case]. Tunis Med; 2006 Sep;84(9):581-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Alpha heavy chain disease. A Tunisian case].
  • [Transliterated title] Maladie des chaines lourdes alpha. A propos d'un cas tunisien.
  • Alpha heavy chain disease is a rare affection in the West and reported mainly in developing countries with the improvement of hygienic conditions, the disease become rare in Tunisia, the last case was reported in 1991.
  • The aim of the study is to report a new Tunisian case and to describe clinical, endoscopical and histological characteristics of the disease.
  • The diagnosis of alpha heavy chain disease was confirmed by histological examination of the resected intestine after surgery for intestinal obstruction.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / diagnosis
  • [MeSH-minor] Adult. Humans. Intestinal Obstruction / etiology. Intestinal Obstruction / surgery. Male

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  • (PMID = 17263208.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Tunisia
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12. Parfenov AI, Krums LM, Sivash ES, Tsaregorodtseva TM, Poleva NI, Ruchkina IN, Sabel'nikova EA, Chikunova BZ: [Algorithm for diagnosis of small intestinal diseases]. Ter Arkh; 2008;80(4):46-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Algorithm for diagnosis of small intestinal diseases].
  • AIM: To review diagnostic approaches in chronic diseases of the small intestine.
  • MATERIAL AND METHODS: A total of 1096 patients with chronic diseases of the small intestine were admitted to the clinic of the Central Research Institute of Gastroenterological Diseases in 1987-2006.
  • RESULTS: Most of the patients (90.5%) had celiac disease, hypolactasia and other types of disaccharidase deficiency, yersiniosis ileitis, Krohn's disease, postresection syndrome of a short small intestine, mesenterial ischemia and endocrine enteropathy.
  • Rare diseases (general variable hypogammaglobulinemia, lymphoma, Wipple's disease and diverticulosis of the small intestine) were diagnosed in 5.8% cases.
  • Primary amyloidosis of the small intestine, eosinophilic gastroenteritis, arteriomesenterial obstruction, primary intestinal pseudoobstruction, hypogammaglobulinemic spru, primary intestinal lymphangiectasia, tuberculosis, total polyposis, Peutz-Eggers and Cronkhite-Canada syndromes, collagenic sprue, erosive-ulcerative jejunoileitis, adenocarcinoma and heavy alpha-chain disease were detected in 3.7% examinees.
  • These diseases were encountered in one to 5 cases for the latest 20 years.
  • CONCLUSION: Clinical diagnosis of small intestinal diseases is based on the syndromes of chronic diarrhea, defective absorption, enteral protein loss, small intestinal obstruction and intestinal hemorrhage.
  • Differential diagnosis of the nosological entities employs x-ray, endoscopic, histological, immunological and other methods.
  • Most of the small intestinal diseases including rare can be diagnosed in any gastroentorological department.
  • [MeSH-major] Algorithms. Endoscopy, Gastrointestinal / methods. Immunologic Tests / methods. Intestinal Diseases / diagnosis. Intestine, Small. Radiography, Abdominal / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 18491580.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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13. Pai RK, Snider WK, Starkey CR, Viswanatha D, Foucar MK, Wilson CS: Nonsecretory variant of immunoproliferative small intestinal disease: a case report with pathologic, immunophenotypic, and molecular findings. Arch Pathol Lab Med; 2005 Nov;129(11):1487-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonsecretory variant of immunoproliferative small intestinal disease: a case report with pathologic, immunophenotypic, and molecular findings.
  • We report a case of the nonsecretory variant of immunoproliferative small intestinal disease involving the distal small bowel and the mesenteric and retroperitoneal lymph nodes in a 19-year-old woman from Mexico.
  • This variant extranodal marginal zone B-cell lymphoma appeared similar in the different sites of involvement, with more interspersed large cells and greater plasmacytic differentiation present in intestinal specimens.
  • Characteristic lymphoepithelial lesions and follicular colonization were seen in intestinal and lymph node sections, respectively.
  • The neoplastic B cells were cytoplasmic immunoglobulin (Ig) A heavy-chain restricted and lacked surface and cytoplasmic light-chain expression by flow cytometric analysis.
  • Molecular studies showed absence of immunoglobulin heavy-chain (IgH) gene rearrangement, with a nonfunctional clonotypic rearrangement of the kappa light-chain gene.
  • This case highlights the role for kappa light-chain gene evaluation in immunoproliferative small intestinal disease, because IgH gene rearrangement analysis is often negative.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / pathology. Lymph Nodes / pathology. Lymphoma, B-Cell, Marginal Zone / pathology
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles. Adult. Amoxicillin / therapeutic use. Anti-Bacterial Agents / therapeutic use. Benzimidazoles / therapeutic use. Drug Therapy, Combination. Female. Gene Rearrangement, B-Lymphocyte, Light Chain / genetics. Humans. Immunophenotyping. Intestine, Small / pathology. Mesentery. Metronidazole / therapeutic use. Omeprazole / analogs & derivatives. Omeprazole / therapeutic use. Retroperitoneal Space. Sulfoxides / therapeutic use

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  • (PMID = 16253033.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Bacterial Agents; 0 / Benzimidazoles; 0 / Sulfoxides; 140QMO216E / Metronidazole; 804826J2HU / Amoxicillin; D8TST4O562 / pantoprazole; KG60484QX9 / Omeprazole
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14. Hara T, Tsurumi H, Kato T, Imao Y, Kojima Y, Kojima K, Kitagawa J, Katsumura N, Araki H, Takami T, Moriwaki H: Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression. Intern Med; 2008;47(4):299-303
MedlinePlus Health Information. consumer health - Intestinal Cancer.

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  • [Title] Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression.
  • A 52-year-old man was admitted to our hospital in October 2001 with abdominal pain.
  • Abdominal X-ray indicated a diagnosis of ileus.
  • Histopathological and immunological examination resulted in a diagnosis of immunoproliferative small intestinal disease (IPSID).
  • He was diagnosed with relapsed IPSID and salvage chemotherapy was started.
  • Immunohistochemical staining revealed T-cell lymphoma.
  • [MeSH-major] Duodenal Neoplasms / etiology. Immunoproliferative Small Intestinal Disease / complications. Lymphoma, T-Cell / etiology
  • [MeSH-minor] Disease Progression. Fatal Outcome. Humans. Male. Middle Aged. Proteins / metabolism

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  • (PMID = 18277034.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proteins
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15. Economidou I, Manousos ON, Triantafillidis JK, Vaslamatzis MM, Zafiropoulou R, Papadakis T: Immunoproliferative small intestinal disease in Greece: presentation of 13 cases including two from Albania. Eur J Gastroenterol Hepatol; 2006 Sep;18(9):1029-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoproliferative small intestinal disease in Greece: presentation of 13 cases including two from Albania.
  • OBJECTIVES: Immunoproliferative small intestinal disease (IPSID) represents a spectrum of clinicopathological entities including alpha-chain disease and other types of lymphoplasmacytic proliferations of the lamina propria of the small intestine, presenting with severe malabsorption.
  • IPSID has been described mainly in the Mediterranean, Middle East, and African countries.
  • METHODS: Current immunological and immunohistochemical methods for the detection of alpha heavy chains and the presence of clonality have been used to study 13 cases of IPSID diagnosed in Greece, two of whom were Albanian residents.
  • RESULTS: The patients were categorized in three subgroups of IPSID: alpha-chain disease (n=8), non-alpha chain disease with other monoclonal immunoglobulins (n=3), and polyclonal 'non-malignant' IPSID (n=2).
  • In several patients the disease had unusual features, and this in some cases delayed the diagnosis.
  • Patients with stage C disease had a short survival, whereas two patients with stage A alpha-chain disease responded to treatment with cyclophosphamide, vincristine and prednisolone, and cyclophosphamide, doxorubicine, vincristine and prednisolone, respectively, have a disease-free long survival of 35 and 12 years, and appear to be cured.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / diagnosis

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  • (PMID = 16894320.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
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16. Liu Z, Takazaki H, Nakazawa Y, Sakato M, Yagi T, Yasunaga T, King SM, Kamiya R: Partially functional outer-arm dynein in a novel Chlamydomonas mutant expressing a truncated gamma heavy chain. Eukaryot Cell; 2008 Jul;7(7):1136-45

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Partially functional outer-arm dynein in a novel Chlamydomonas mutant expressing a truncated gamma heavy chain.
  • The outer dynein arm of Chlamydomonas flagella contains three heavy chains (alpha, beta, and gamma), each of which exhibits motor activity.
  • Here we report the isolation of a novel mutant, oda2-t, whose gamma heavy chain is truncated at about 30% of the sequence.
  • While the previously isolated gamma chain mutant oda2 lacks the entire outer arm, oda2-t retains outer arms that contain alpha and beta heavy chains, suggesting that the N-terminal sequence (corresponding to the tail region) is necessary and sufficient for stable outer-arm assembly.
  • Thin-section electron microscopy and image analysis localize the gamma heavy chain to a basal region of the outer-arm image in the axonemal cross section.
  • The motility of oda2-t is lower than that of the wild type and oda11 (lacking the alpha heavy chain) but higher than that of oda2 and oda4-s7 (lacking the motor domain of the beta heavy chain).
  • Thus, the outer-arm dynein lacking the gamma heavy-chain motor domain is partially functional.
  • The availability of mutants lacking individual heavy chains should greatly facilitate studies on the structure and function of the outer-arm dynein.

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  • (PMID = 18487347.001).
  • [ISSN] 1535-9786
  • [Journal-full-title] Eukaryotic cell
  • [ISO-abbreviation] Eukaryotic Cell
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM051293; United States / NIGMS NIH HHS / GM / GM51293
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Subunits; 0 / Protozoan Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.4.2 / Dyneins
  • [Other-IDs] NLM/ PMC2446680
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17. Ishikawa T, Sakakibara H, Oiwa K: The architecture of outer dynein arms in situ. J Mol Biol; 2007 May 18;368(5):1249-58

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Outer dynein arms, the force generators for axonemal motion, form arrays on microtubule doublets in situ, although they are bouquet-like complexes with separated heads of multiple heavy chains when isolated in vitro.
  • To understand how the three heavy chains are folded in the array, we reconstructed the detailed 3D structure of outer dynein arms of Chlamydomonas flagella in situ by electron cryo-tomography and single-particle averaging.
  • The three AAA rings of heavy chains, seen as stacked plates, are connected in a striking manner on microtubule doublets.
  • The tail of the alpha-heavy chain, identified by analyzing the oda11 mutant, which lacks alpha-heavy chain, extends from the AAA ring tilted toward the tip of the axoneme and towards the inside of the axoneme at 50 degrees , suggesting a three-dimensional power stroke.
  • The neighboring outer dynein arms are connected through two filamentous structures: one at the exterior of the axoneme and the other through the alpha-tail.
  • Although the beta-tail seems to merge with the alpha-tail at the internal side of the axoneme, the gamma-tail is likely to extend at the exterior of the axoneme and join the AAA ring.
  • This suggests that the fold and function of gamma-heavy chain are different from those of alpha and beta-chains.

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  • (PMID = 17391698.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.6.4.2 / Dyneins
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18. Zhou H, Hickford JG, Fang Q: Polymorphism of the IGHA gene in sheep. Immunogenetics; 2005 Jul;57(6):453-7
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  • In this study, variation in the immunoglobulin heavy alpha chain constant gene (IGHA) of sheep was investigated by amplification of a fragment that included the hinge coding sequence, followed by single-strand conformational polymorphism (SSCP) analysis and DNA sequencing.
  • [MeSH-major] Immunoglobulin alpha-Chains / genetics. Polymorphism, Single-Stranded Conformational. Sheep / immunology

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  • (PMID = 16025324.001).
  • [ISSN] 0093-7711
  • [Journal-full-title] Immunogenetics
  • [ISO-abbreviation] Immunogenetics
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY956424/ AY956425/ AY956426
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Immunoglobulin alpha-Chains
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19. Furuta A, Yagi T, Yanagisawa HA, Higuchi H, Kamiya R: Systematic comparison of in vitro motile properties between Chlamydomonas wild-type and mutant outer arm dyneins each lacking one of the three heavy chains. J Biol Chem; 2009 Feb 27;284(9):5927-35

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic comparison of in vitro motile properties between Chlamydomonas wild-type and mutant outer arm dyneins each lacking one of the three heavy chains.
  • Outer arm dynein (OAD) of cilia and flagella contains two or three distinct heavy chains, each having a motor function.
  • To elucidate their functional difference, we compared the in vitro motile properties of Chlamydomonas wild-type OAD containing the alpha, beta, and gamma heavy chains and three kinds of mutant OADs, each lacking one of the three heavy chains.
  • Wild-type OAD displayed microtubule gliding in the presence of ATP and ADP, with a maximal velocity of 5.0 mum/s, which is approximately 1/4 of the microtubule sliding velocity in the axoneme.
  • The absence of the beta heavy chain lowered both the gliding velocity and ATPase activity, whereas the absence of the gamma heavy chain increased both activities.
  • Strikingly, the absence of the alpha heavy chain lowered the gliding velocity but increased the ATPase activity.
  • Thus, the three heavy chains are likely to play distinct roles and regulate each other to achieve coordinated force production.

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  • (PMID = 19124458.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Subunits; EC 3.6.4.2 / Dyneins
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20. Lin YS, Zhou H, Forrest RH, Frampton CM, Hickford JG: Association between variation in faecal egg count for a mixed field-challenge of nematode parasites and IGHA gene polymorphism. Vet Immunol Immunopathol; 2009 Apr 15;128(4):389-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Research has shown that variation in ovine immunoglobulin A (IgA) levels are associated with reduced faecal egg counts (FECs) in sheep hosting gastro-intestinal (GI) parasites.
  • Variation in the constant region of the ovine IgA heavy alpha chain gene (IGHA) may result in structurally and functionally different IgA molecules and may consequently lead to variation in the IgA response to parasitisation.
  • However, when the data was split into predominant challenge type groups, associations were detected.
  • [MeSH-major] Gastrointestinal Diseases / veterinary. Immunoglobulin A / genetics. Nematoda / growth & development. Nematode Infections / veterinary. Sheep Diseases / immunology. Sheep Diseases / parasitology
  • [MeSH-minor] Alleles. Animals. DNA, Helminth / chemistry. DNA, Helminth / genetics. Feces / parasitology. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Heavy Chains / immunology. Male. Parasite Egg Count / veterinary. Polymerase Chain Reaction / veterinary. Polymorphism, Single-Stranded Conformational. Sheep

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  • (PMID = 19150137.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA, Helminth; 0 / Immunoglobulin A; 0 / Immunoglobulin Heavy Chains
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21. Quinn BA, Hayes MA, Waelchli RO, Kennedy MW, Betteridge KJ: Changes in major proteins in the embryonic capsule during immobilization (fixation) of the conceptus in the third week of pregnancy in the mare. Reproduction; 2007 Jul;134(1):161-70
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  • During fixation, beta2M in the capsule underwent limited proteolysis to an approximately 8 kDa form lacking nine amino acids from the N terminus, and was subsequently degraded.
  • During this period, beta2M in the capsule was evidently not part of a complex with major histocompatibility complex class 1 heavy alpha chain bands because these were undetectable in the capsule and uterine lavage.
  • These studies indicate that intact beta2M is a major protein associated with the embryonic capsule before fixation, after which it undergoes limited proteolysis to a truncated approximately 8 kDa form that remains in the capsule after the conceptus is immobilized.
  • [MeSH-minor] Animals. Electrophoresis, Polyacrylamide Gel. Female. Gene Expression. Gestational Age. Histocompatibility Antigens Class I / genetics. Histocompatibility Antigens Class I / metabolism. Immunoblotting. Pregnancy. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Uteroglobin / analysis. Uteroglobin / metabolism. Uterus / chemistry. Uterus / metabolism. Yolk Sac / chemistry. Yolk Sac / metabolism. beta 2-Microglobulin / analysis. beta 2-Microglobulin / metabolism

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  • (PMID = 17641098.001).
  • [ISSN] 1470-1626
  • [Journal-full-title] Reproduction (Cambridge, England)
  • [ISO-abbreviation] Reproduction
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / Histocompatibility Antigens Class I; 0 / MHC class I-related chain A; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 9060-09-7 / Uteroglobin
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22. Lampton PW, Goldstein CY, Warner CM: The role of tapasin in MHC class I protein trafficking in embryos and T cells. J Reprod Immunol; 2008 Jun;78(1):28-39
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • Similar in structure to MHC class Ia proteins, Qa-2 protein is a trimer of the alpha (heavy) chain, beta(2) microglobulin and a bound peptide.

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  • (PMID = 18061684.001).
  • [ISSN] 0165-0378
  • [Journal-full-title] Journal of reproductive immunology
  • [ISO-abbreviation] J. Reprod. Immunol.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD039215-05; United States / NICHD NIH HHS / HD / R01 HD039215; United States / NICHD NIH HHS / HD / HD39215; United States / NICHD NIH HHS / HD / R01 HD039215-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Molecular Chaperones; 0 / Peptides; 0 / Q surface antigens; 0 / Tap1 protein, mouse; 0 / beta 2-Microglobulin
  • [Other-IDs] NLM/ NIHMS51787; NLM/ PMC2459227
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23. Wahner-Roedler DL, Kyle RA: Heavy chain diseases. Best Pract Res Clin Haematol; 2005;18(4):729-46
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  • [Title] Heavy chain diseases.
  • Heavy chain diseases (HCDs) are rare B-cell lymphoplasma-cell proliferative disorders characterized by production of truncated monoclonal immunoglobulin heavy chains without associated light chains.
  • HCDs involving the three main immunoglobulin classes have been described; alpha-HCD is the most common and has the most uniform presentation, gamma- and mu-HCDs have variable clinical presentations and histopathologic features.
  • HCDs can be thought of as variant types of non-Hodgkin lymphoma: alpha-HCD presents as an extranodal marginal-zone lymphoma of mucosa-associated lymph-node tissue, gamma-HCD as lymphoplasmacytoid non-Hodgkin lymphoma, and mu-HCD as small lymphocytic non-Hodgkin lymphoma or chronic lymphocytic leukemia.
  • Diagnosis of HCD requires documentation of a deleted immunoglobulin heavy chain without a bound light chain in the serum or urine.
  • Prognosis is variable, and no standardized effective treatment programs are available except for alpha-HCD, which in its early stage may respond to antibiotics.
  • [MeSH-major] Heavy Chain Disease / diagnosis
  • [MeSH-minor] Clinical Laboratory Techniques. Humans. Immunoglobulin Heavy Chains / genetics. Lymphoproliferative Disorders / etiology. Prognosis

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  • (PMID = 16026747.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
  • [Number-of-references] 38
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24. Salem PA, Estephan FF: Immunoproliferative small intestinal disease: current concepts. Cancer J; 2005 Sep-Oct;11(5):374-82
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for immunoproliferative small intestinal disease .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoproliferative small intestinal disease: current concepts.
  • Immunoproliferative small intestinal disease is a distinctive lymphoproliferative disorder.
  • Among these disorders, it is the only disease associated with a specific and characteristic abnormal protein, and also an identifiable, at least in some patients, early phase with a benign-looking histo-pathologic expression.
  • Whether the disease at this stage is malignant or not is not known.
  • This observation is significant and raises the question of chemoprevention in lymphomas.
  • In contrast to primary nonimmunoproliferative small intestinal lymphomas, in which the pathology in the intestine is usually focal and involving specific segments of the intestine and leaving the segments between the involved areas free of disease, the pathology in immunoproliferative small intestinal disease is diffuse, with a mucosal cellular infiltrate involving large segments of the intestine and sometimes the entire length of the intestine, thus producing malabsorption.
  • Preliminary recent epidemiological data have shown a decrease in the incidence of this disease in endemic areas, and therefore environmental factors are suspected to play a major role in its pathogenesis.
  • Additional research is indicated not only to understand this specific lymphoproliferative disorder but also to understand lymphomas in general.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease

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  • (PMID = 16259867.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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25. Miron I, Mihăilă D, Aprodu G, Miron L, Plămădeală P, Moisă SM: Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy. Rom J Morphol Embryol; 2009;50(4):733-8
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  • [Title] Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy.
  • The authors present a case of colonic monoblastic sarcoma, previously treated for other digestive abnormalities (malabsorbtion, Hirschprung's disease).
  • Important similitudes with immunoproliferative small intestinal disease (IPSID) lymphoma were demonstrated for this patient (male, 2-year-old).
  • Some particularities of this case are the young age and the extremely rapid development of the malignant disease in a patient with no previous signs of acute non-lymphoblastic leukemia.
  • The initial diagnosis was of malabsorbtion syndrome, based on the clinical exam at presentation, and then the patient was thought to have a form of Hirschprung's disease, due to a functional intestinal disorder (slow transit).
  • After the necropsy, pathologists diagnosed an immunoproliferative small intestinal disease, and four years later, they performed a more appropriate pathological exam, which explained better clinical symptoms associated to this complex case.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Immunoproliferative Small Intestinal Disease / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Hirschsprung Disease / diagnosis. Humans. Malabsorption Syndromes / diagnosis. Male

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  • (PMID = 19942975.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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26. Evan AP, Bledsoe S, Worcester EM, Coe FL, Lingeman JE, Bergsland KJ: Renal inter-alpha-trypsin inhibitor heavy chain 3 increases in calcium oxalate stone-forming patients. Kidney Int; 2007 Dec;72(12):1503-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Renal inter-alpha-trypsin inhibitor heavy chain 3 increases in calcium oxalate stone-forming patients.
  • Inter-alpha-trypsin inhibitor heavy-chain proteins bind to the protease inhibitor bikunin and to hyaluronan, stabilizes extracellular matrix in various tissues, and also inhibits calcium oxalate crystallization in vitro.
  • In both normal and stone-forming patients, we found heavy chain 3 and hyaluronan in the interstitial matrix of the kidney.
  • In stone formers, heavy chain 3 was also present in collecting duct, thin loop, and interstitial cells.
  • Heavy chain 3 and osteopontin colocalized in plaque matrix and urothelial cells.
  • Within individual plaque spherules, heavy chain 3 was found in the matrix layer while osteopontin was located along the crystal-matrix interface.
  • Bikunin was present only in the collecting duct apical membranes and the loop cell cytoplasm of stone formers colocalizing with osteopontin and heavy chain 3.
  • Widespread heavy chain 3 was only present in stone formers, whereas osteopontin was similarly expressed in normal and stone-forming subjects except for its localization in plaques of the stone formers.
  • This is consistent with studies linking inter-alpha-trypsin inhibitor components to human stone disease, although their role is still unclear.
  • Heavy chain 3 may also play a role in stabilizing hyaluronan in the renal interstitial matrix.
  • [MeSH-major] Alpha-Globulins / metabolism. Calcium Oxalate / urine. Urinary Calculi / metabolism

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  • (PMID = 17898697.001).
  • [ISSN] 0085-2538
  • [Journal-full-title] Kidney international
  • [ISO-abbreviation] Kidney Int.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P01 DK56788
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / alpha-1-microglobulin; 106441-73-0 / Osteopontin; 2612HC57YE / Calcium Oxalate; 39346-44-6 / inter-alpha-inhibitor; 9004-61-9 / Hyaluronic Acid
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27. Al-Saleem T, Al-Mondhiry H: Immunoproliferative small intestinal disease (IPSID): a model for mature B-cell neoplasms. Blood; 2005 Mar 15;105(6):2274-80
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for immunoproliferative small intestinal disease .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoproliferative small intestinal disease (IPSID): a model for mature B-cell neoplasms.
  • Immunoproliferative small intestinal disease (IPSID) was recently added to the growing list of infectious pathogen-associated human lymphomas.
  • IPSID is a variant of the B-cell lymphoma of mucosa-associated lymphoid tissue (MALT), which involves mainly the proximal small intestine resulting in malabsorption, diarrhea, and abdominal pain.
  • Geographically, IPSID is most prevalent in the Middle East and Africa.
  • IPSID lymphomas reveal excessive plasma cell differentiation and produce truncated alpha heavy chain proteins lacking the light chains as well as the first constant domain.
  • The corresponding mRNA lacks the variable heavy chain (V(H)) and the constant heavy chain 1 (C(H)1) sequences and contains deletions as well as insertions of unknown origin.
  • Cytogenetic studies demonstrated clonal rearrangements involving predominantly the heavy and light chain genes, including t(9;14) translocation involving the PAX5 gene.
  • Early-stage IPSID responds to antibiotics (30%-70% complete remission).
  • Most untreated IPSID patients progress to lymphoplasmacytic and immunoblastic lymphoma invading the intestinal wall and mesenteric lymph nodes, and may metastasize to a distant organ.
  • IPSID lymphoma shares clinical, morphologic, and molecular features with MALT lymphoma, lymphoplasmacytic lymphoma, and plasma cell neoplasms.
  • [MeSH-major] Campylobacter Infections. Campylobacter jejuni. Immunoproliferative Small Intestinal Disease. Lymphoma, B-Cell, Marginal Zone. Plasma Cells / immunology
  • [MeSH-minor] Adolescent. Adult. Africa. B-Cell-Specific Activator Protein / genetics. B-Cell-Specific Activator Protein / immunology. Child. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 9 / genetics. Chromosomes, Human, Pair 9 / immunology. Female. Humans. Immunoglobulin Light Chains / genetics. Immunoglobulin Light Chains / immunology. Immunoglobulin Variable Region / genetics. Immunoglobulin Variable Region / immunology. Immunoglobulin alpha-Chains / genetics. Immunoglobulin alpha-Chains / immunology. Intestine, Small / immunology. Intestine, Small / pathology. Lymph Nodes / immunology. Lymph Nodes / pathology. Male. Mesentery / immunology. Mesentery / pathology. Middle East. Sequence Deletion / genetics. Sequence Deletion / immunology. Translocation, Genetic / genetics. Translocation, Genetic / immunology

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  • (PMID = 15542584.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Immunoglobulin Light Chains; 0 / Immunoglobulin Variable Region; 0 / Immunoglobulin alpha-Chains; 0 / PAX5 protein, human
  • [Number-of-references] 78
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28. Du MQ: MALT lymphoma : recent advances in aetiology and molecular genetics. J Clin Exp Hematop; 2007 Nov;47(2):31-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MALT lymphoma : recent advances in aetiology and molecular genetics.
  • Mucosa-associated lymphoid tissue (MALT) lymphoma is a common low grade B-cell lymphoma arising from a background of chronic inflammatory disease at a number of mucosal sites.
  • Those originating in the stomach are causatively linked to Helicobacter pylori infection and eradication of the bacterium with antibiotics leads to long-term complete regression of the lymphoma in aproximately 70% of cases.
  • Now, there is further evidence of linking Campylobacter jejuni, Borrelia burgdorferi and Chlamydia psittaci infection with immunoproliferative small intestine disease, MALT lymphoma of the skin and ocular adnexa respectively. t(11;18)/API2-MALT1, t(1;14)/IGH-BCL10, t(14;18)/IGH-MALT1 and t(3;14)/IGH-FOXP1 occur at considerably variable incidences in MALT lymphomas of different sites.
  • The first three chromosome translocations are specifically associated with the MALT lymphoma entity and the oncogenic products of these translocations have been shown to target a common molecular pathway, i.e. the nuclear factor-kappaB pathway.
  • Here, I review the recent advances in our understanding of the association of microbial pathogens with MALT lymphoma of various sites and the molecular genetics underlying the lymphoma development.
  • [MeSH-major] Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / microbiology

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  • (PMID = 18040143.001).
  • [ISSN] 1346-4280
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Number-of-references] 99
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29. Lowey S, Lesko LM, Rovner AS, Hodges AR, White SL, Low RB, Rincon M, Gulick J, Robbins J: Functional effects of the hypertrophic cardiomyopathy R403Q mutation are different in an alpha- or beta-myosin heavy chain backbone. J Biol Chem; 2008 Jul 18;283(29):20579-89
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  • [Title] Functional effects of the hypertrophic cardiomyopathy R403Q mutation are different in an alpha- or beta-myosin heavy chain backbone.
  • The R403Q mutation in the beta-myosin heavy chain (MHC) was the first mutation to be linked to familial hypertrophic cardiomyopathy (FHC), a primary disease of heart muscle.
  • The introduction of the mouse model for FHC (the mouse expresses predominantly alpha-MHC as opposed to the beta-isoform in larger mammals) created a new paradigm for FHC based on finding enhanced motor function for R403Q alpha-MHC.
  • To help resolve these conflicting mechanisms, we used a transgenic mouse model in which the endogenous alpha-MHC was largely replaced with transgenically encoded beta-MHC.
  • A His(6) tag was cloned at the N terminus of the alpha-and beta-MHC to facilitate protein isolation by Ni(2+)-chelating chromatography.
  • Characterization of the R403Q alpha-MHC by the in vitro motility assay showed a 30-40% increase in actin filament velocity compared with wild type, consistent with published studies.
  • We find that the actin-activated MgATPase activity for R403Q alpha-S1 is approximately 30% higher than for wild type, whereas the enzymatic activity for R403Q beta-S1 is reduced by approximately 10%.

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  • (PMID = 18480046.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL 087862; United States / NHLBI NIH HHS / HL / HL 077101; United States / NHLBI NIH HHS / HL / HL 074728; United States / NHLBI NIH HHS / HL / HL 69799; United States / NCRR NIH HHS / RR / P20 RR 16435; United States / NHLBI NIH HHS / HL / HL 59408; United States / NIAMS NIH HHS / AR / AR 053975
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 721M9407IY / Propylthiouracil; 94ZLA3W45F / Arginine; EC 3.6.1.- / Ca(2+) Mg(2+)-ATPase; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ PMC2459289
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30. Poutanen T, Tikanoja T, Jääskeläinen P, Jokinen E, Silvast A, Laakso M, Kuusisto J: Diastolic dysfunction without left ventricular hypertrophy is an early finding in children with hypertrophic cardiomyopathy-causing mutations in the beta-myosin heavy chain, alpha-tropomyosin, and myosin-binding protein C genes. Am Heart J; 2006 Mar;151(3):725.e1-725.e9
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  • [Title] Diastolic dysfunction without left ventricular hypertrophy is an early finding in children with hypertrophic cardiomyopathy-causing mutations in the beta-myosin heavy chain, alpha-tropomyosin, and myosin-binding protein C genes.
  • METHODS: All children (aged 1.5-16.7 years) from 14 HCM families with identified disease-causing mutations (the Arg719Trp mutation in the beta-myosin heavy chain gene [MYH7], the Asp175Asn mutation in the alpha-tropomyosin gene [TPM1], the Gln1061X mutation in the myosin-binding protein C gene [MYBPC3], and the IVS5-2A-->C mutation in the MYBPC3 gene) and 53 matched control children were examined with electrocardiography and 2- and 3-dimensional echocardiography (2DE and 3DE).
  • RESULTS: Of 53 children from HCM families, 27 (51%) had a disease-causing mutation (G+).
  • CONCLUSIONS: In children with HCM-causing mutations, signs of diastolic dysfunction are found in about half of the cases, as LVH is present only in small percentage of these children.

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  • (PMID = 16504640.001).
  • [ISSN] 1097-6744
  • [Journal-full-title] American heart journal
  • [ISO-abbreviation] Am. Heart J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / TPM1 protein, human; 0 / Tropomyosin; 0 / myosin-binding protein C; 85637-73-6 / Atrial Natriuretic Factor; EC 3.6.1.- / Ventricular Myosins
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31. Stratigos P, Kouskos E, Kouroglou M, Chrisafis I, Fois L, Mavrogiorgis A, Axiotis E, Zamtrakis S: Emergency pancreatoduodenectomy (whipple procedure) for massive upper gastrointestinal bleeding caused by a diffuse B-cell lymphoma of the duodenum: report of a case. Surg Today; 2007;37(8):680-4
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  • [Title] Emergency pancreatoduodenectomy (whipple procedure) for massive upper gastrointestinal bleeding caused by a diffuse B-cell lymphoma of the duodenum: report of a case.
  • We herein report a rare case of a massive upper gastrointestinal (GI) bleeding, caused by high-grade diffuse B-cell lymphoma of the duodenum, secondary to immunoproliferative small intestinal disease (IPSID) and treated with an emergency partial pancreatoduodenectomy.
  • An urgent abdominal ultrasound raised the suspicion of a large, possibly bleeding, neoplasm of the duodenum, which was finally confirmed by abdominal computed tomography.
  • Histologically, the tumor was a high-grade B-cell lymphoma of the duodenum.
  • The nearby small intestinal mucosa was suggestive of IPSID.
  • A massive upper GI hemorrhage from a high-grade B-cell non-Hodgkin lymphoma of the duodenum, which develops secondary to IPSID, is a very rare clinical demonstration of this disease.
  • [MeSH-major] Duodenal Neoplasms / complications. Emergency Treatment. Gastrointestinal Hemorrhage / surgery. Lymphoma, B-Cell / complications. Pancreaticoduodenectomy / methods. Upper Gastrointestinal Tract / surgery
  • [MeSH-minor] Humans. Immunoproliferative Small Intestinal Disease

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  • (PMID = 17643214.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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32. Mutanabbi M, Noor MK, Helal MA, Rahman MH: Coeliac disease. Mymensingh Med J; 2009 Jan;18(1 Suppl):S136-139
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  • [Title] Coeliac disease.
  • Coeliac disease is an autoimmune disorder of the small bowel that occurs in genetically predisposed people of all ages from middle infancy.
  • Coeliac disease is caused by a reaction to gliadin, a gluten protein found in wheat.
  • Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the protein and the immune system cross reacts with the bowel tissue, causing an inflammatory reaction that leads to flattening of the lining of the small intestine, which interferes with the absorption of nutrient's.
  • He had loose mucoid stool, abdominal distension, bloating and history of loss of weight for two years.
  • Along with the routine examinations foecal fat estimation, MT, USG of whole abdomen, Barium follow through, endoscopic biopsy and tissue transglutaminage IgA autoantibody was done.
  • Histopathological report was in favour of immunoproliferative small intestinal disease.
  • Tissue transglutaminage IgA autoantibody was in higher level though done in a gluten free state.
  • Symptoms of diarrhoea, abdominal distention and bloatedness gradually decreased.
  • For patients presenting with alteration of bowel habit, abdominal distension, bloating and history of weight loss for long time, the importance of considering coeliac diseases as a differential diagnosis cannot be overemphasized.

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  • (PMID = 19377424.001).
  • [ISSN] 1022-4742
  • [Journal-full-title] Mymensingh medical journal : MMJ
  • [ISO-abbreviation] Mymensingh Med J
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Bangladesh
  • [Chemical-registry-number] 0 / Immunoglobulin A; 9007-90-3 / Gliadin; EC 2.3.2.13 / Transglutaminases
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33. Narolska NA, Eiras S, van Loon RB, Boontje NM, Zaremba R, Spiegelen Berg SR, Stooker W, Huybregts MA, Visser FC, van der Velden J, Stienen GJ: Myosin heavy chain composition and the economy of contraction in healthy and diseased human myocardium. J Muscle Res Cell Motil; 2005;26(1):39-48
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  • [Title] Myosin heavy chain composition and the economy of contraction in healthy and diseased human myocardium.
  • Changes in myosin heavy chain (MHC) isoform expression and protein composition occur during cardiac disease and it has been suggested that even a minor shift in MHC composition may exert a considerable effect on myocardial energetics and performance.
  • Atrial fibrillation was accompanied by a significant shift from the fast alpha-MHC isoform to the slow beta-MHC isoform, whereas both donor and failing ventricular tissue contained almost exclusively the beta-MHC isoform.
  • [MeSH-major] Arrhythmia, Sinus / physiopathology. Atrial Fibrillation / physiopathology. Heart / physiopathology. Myocardial Contraction. Myocardium / metabolism. Myosin Heavy Chains / metabolism
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Biopsy. Chronic Disease. Electrophoresis, Polyacrylamide Gel. Female. Humans. Male. Protein Isoforms / analysis. Protein Isoforms / genetics. Protein Isoforms / metabolism


34. Rundell VL, Manaves V, Martin AF, de Tombe PP: Impact of beta-myosin heavy chain isoform expression on cross-bridge cycling kinetics. Am J Physiol Heart Circ Physiol; 2005 Feb;288(2):H896-903
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  • [Title] Impact of beta-myosin heavy chain isoform expression on cross-bridge cycling kinetics.
  • Myosin heavy chain (MHC) isoforms alpha and beta have intrinsically different ATP hydrolysis activities (ATPase) and therefore cross-bridge cycling rates in solution.
  • There is considerable evidence of altered MHC expression in rodent cardiac disease models; however, the effect of incremental beta-MHC expression over a wide range on the rate of high-strain, isometric cross-bridge cycling is yet to be ascertained.
  • We treated male rats with 6-propyl-2-thiouracil (PTU; 0.8 g/l in drinking water) for short intervals (6, 11, 16, and 21 days) to generate cardiac MHC patterns in transition from predominantly alpha-MHC to predominantly beta-MHC.
  • MHC isoform content in each experimental muscle was measured by SDS-PAGE and densitometry. alpha-MHC content decreased significantly and progressively with length of PTU treatment [68 +/- 5%, 58 +/- 4%, 37 +/- 4%, and 27 +/- 6% for 6, 11, 16, and 21 days, respectively; P < 0.001 (ANOVA)].
  • Tension cost decreased, linearly, with decreased alpha-MHC content [6.7 +/- 0.4, 5.6 +/- 0.5, 4.0 +/- 0.4, and 3.9 +/- 0.3 ATPase/tension for 6, 11, 16, and 21 days, respectively; P < 0.001 (ANOVA)].
  • Likewise, ktr was significantly and progressively depressed with length of PTU treatment [11.1 +/- 0.6, 9.1 +/- 0.5, 8.2 +/- 0.7, and 6.2 +/- 0.3 s(-1) for 6, 11, 16, and 21 days, respectively; P < 0.05 (ANOVA)] Thus cross-bridge cycling, under high strain, for alpha-MHC is three times higher than for beta-MHC.
  • Furthermore, under isometric conditions, alpha-MHC and beta-MHC cross bridges hydrolyze ATP independently of one another.
  • [MeSH-major] Hypothyroidism / metabolism. Myocardial Contraction / physiology. Myocytes, Cardiac / metabolism. Myosin Heavy Chains / metabolism

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  • (PMID = 15471982.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-64942; United States / NHLBI NIH HHS / HL / HL-P01-62426; United States / NHLBI NIH HHS / HL / HL/DK-R01-63704; United States / NHLBI NIH HHS / HL / T32-HL-072742; United States / NHLBI NIH HHS / HL / T32-HL-07692
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antithyroid Agents; 0 / Bmyo protein, rat; 721M9407IY / Propylthiouracil; 8L70Q75FXE / Adenosine Triphosphate; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
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35. Magdelaine-Beuzelin C, Vermeire S, Goodall M, Baert F, Noman M, Assche GV, Ohresser M, Degenne D, Dugoujon JM, Jefferis R, Rutgeerts P, Lefranc MP, Watier H: IgG1 heavy chain-coding gene polymorphism (G1m allotypes) and development of antibodies-to-infliximab. Pharmacogenet Genomics; 2009 May;19(5):383-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IgG1 heavy chain-coding gene polymorphism (G1m allotypes) and development of antibodies-to-infliximab.
  • OBJECTIVE: The chimeric anti-tumor necrosis factor-alpha antibody infliximab is known to induce antibodies-to-infliximab (ATI) in some treated patients.
  • Immunogenicity in murine variable domains is expected; however, constant domains of its human heavy gamma1 chain may also be implicated as it expresses G1m1 and G1m17 allotypes.
  • This allelic form may be immunogenic in patients that are homozygous for the G1m3 allotype commonly expressed in Caucasoid populations.
  • Two hundred forty-five blood donors and 118 previously described patients suffering from Crohn's disease, treated with infliximab, and having developed ATI in 73 of them, were genotyped.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibody Formation / genetics. Immunoglobulin G / genetics. Immunoglobulin Heavy Chains / genetics
  • [MeSH-minor] Anti-Inflammatory Agents / immunology. Anti-Inflammatory Agents / therapeutic use. Case-Control Studies. Cohort Studies. Crohn Disease / blood. Crohn Disease / drug therapy. Crohn Disease / genetics. Crohn Disease / immunology. Gene Frequency. Genotype. Humans. Immunoglobulin Allotypes / genetics. Infliximab. Models, Molecular

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  • (PMID = 19319024.001).
  • [ISSN] 1744-6872
  • [Journal-full-title] Pharmacogenetics and genomics
  • [ISO-abbreviation] Pharmacogenet. Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Allotypes; 0 / Immunoglobulin G; 0 / Immunoglobulin Heavy Chains; B72HH48FLU / Infliximab
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36. Song J, Patel M, Rosenzweig CN, Chan-Li Y, Sokoll LJ, Fung ET, Choi-Miura NH, Goggins M, Chan DW, Zhang Z: Quantification of fragments of human serum inter-alpha-trypsin inhibitor heavy chain 4 by a surface-enhanced laser desorption/ionization-based immunoassay. Clin Chem; 2006 Jun;52(6):1045-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantification of fragments of human serum inter-alpha-trypsin inhibitor heavy chain 4 by a surface-enhanced laser desorption/ionization-based immunoassay.
  • BACKGROUND: Several proteolytically derived fragments from the proline-rich region (PRR) of human inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) have been identified by surface-enhanced or matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS or MALDI-TOF-MS) as potential disease markers.
  • In this study, we used this high-throughput approach to quantify and characterize the extensive fragmentation within the PRR of human serum ITIH4 and determined its association with different disease conditions.
  • RESULTS: Human serum ITIH4 was shown to be extensively proteolytically processed within the PRR, and its fragmentation patterns were closely associated with different disease conditions.
  • CONCLUSIONS: The fragmentation patterns within the PRR of human serum ITIH4 are associated with different disease conditions and may hold important diagnostic information.

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  • (PMID = 16574760.001).
  • [ISSN] 0009-9147
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P50 CA83639; United States / NCI NIH HHS / CA / CA115102-01; United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Blood Proteins; 0 / Glycoproteins; 0 / ITIH4 protein, human; 0 / Proteinase Inhibitory Proteins, Secretory
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37. Qin W, Feng J, Li Y, Lin Z, Shen B: A novel domain antibody rationally designed against TNF-alpha using variable region of human heavy chain antibody as scaffolds to display antagonistic peptides. Mol Immunol; 2007 Mar;44(9):2355-61
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  • [Title] A novel domain antibody rationally designed against TNF-alpha using variable region of human heavy chain antibody as scaffolds to display antagonistic peptides.
  • Neutralizing of TNF-alpha has been proved effective in treatment of some autoimmune diseases, e.g. rheumatoid arthritis and Crohn's disease.
  • Low molecular weight synthetic peptides can mimic the binding sites of TNF-alpha receptors and block the activity of TNF-alpha.
  • In order to stabilize the conformation, increase the affinity and bioactivity, in this study, heavy chain variable region of human antibody was used as a scaffold to simultaneously display three peptides, which were designed on the interaction between TNF-alpha and it's neutralizing monoclonal antibody.
  • On the basis of the structural character and physical-chemical property of the families of seven kinds of heavy chain variable regions (VH) in human antibodies, the fifth type of VH was screened as scaffold to display the antagonist peptide.
  • Based on the computer-guided molecular design method, a novel domain antibody against TNF-alpha (named as ATD5) was designed as TNF-alpha antagonist.
  • The binding activity with TNF-alpha was higher than free peptides.
  • After expression and purification in Escherichia coli, ATD5 could bind directly with TNF-alpha and inhibit the binding of TNF-alpha to its two receptors, TNFR1 and TNFR2.
  • ATD5 could also reduce the TNF-alpha-mediated cytotoxicity and inhibit TNF-alpha-mediated caspase activation on L929 cells in a dose dependent manner.
  • This study provides a novel strategy for the development of new TNF-alpha inhibitors.
  • This study demonstrates that it is possible to screen potential antagonists of TNF-alpha using in vitro analysis systems in combination with the computer-aided modeling method.
  • [MeSH-major] Antibodies, Monoclonal / chemistry. Antibodies, Monoclonal / immunology. Immunoglobulin Heavy Chains / immunology. Immunoglobulin Variable Region / immunology. Peptides / pharmacology. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Amino Acid Sequence. Animals. Antibodies, Blocking / immunology. Antigen-Antibody Reactions / drug effects. Antigen-Antibody Reactions / immunology. Caspases / metabolism. Cytotoxicity, Immunologic / drug effects. Enzyme Activation / drug effects. Humans. Mice. Models, Molecular. Molecular Sequence Data. Mutant Proteins / metabolism. Protein Structure, Tertiary / drug effects. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism

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  • (PMID = 17125837.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Blocking; 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Mutant Proteins; 0 / Peptides; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspases
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38. Martin AF, Bhatti S, Pyne-Geithman GJ, Farjah M, Manaves V, Walker L, Franks R, Strauch AR, Paul RJ: Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle. Am J Physiol Cell Physiol; 2007 Jul;293(1):C238-45
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  • [Title] Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle.
  • Their proportion changes with development, hormonal status and disease, but their function is unknown.
  • We developed mice carrying the myosin heavy chain (MyHC) transgenes SM1, cMyc-tagged SM1, SM2, and V5-tagged SM2, and all transgenes corresponded to the SMa NH(2)-terminal isoform.
  • Transgene expression was targeted to smooth muscle by the smooth muscle alpha-actin promoter.
  • Despite significant protein expression of tagged MyHCs we found only small changes in the SM1:SM2 protein ratio.
  • We hypothesize that small changes in the SM1:SM2 ratio could be amplified if they are associated with changes in thick filament assembly and underlie the altered contractility.
  • [MeSH-major] Aorta / metabolism. Gene Expression. Muscle, Smooth / metabolism. Myosin Heavy Chains / metabolism. Smooth Muscle Myosins / metabolism. Urinary Bladder / metabolism

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  • (PMID = 17392380.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-64942
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / smooth muscle actin, rat; 660YQ98I10 / Potassium Chloride; EC 3.6.1.- / Smooth Muscle Myosins; EC 3.6.4.1 / Myosin Heavy Chains
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39. Dyer MJ, Akasaka T, Capasso M, Dusanjh P, Lee YF, Karran EL, Nagel I, Vater I, Cario G, Siebert R: Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers? Blood; 2010 Feb 25;115(8):1490-9
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  • [Title] Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers?
  • Chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus define common subgroups of B-cell lymphoma but are rare in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • The possible clinical importance of many of the various IGH translocations in BCP-ALL remains to be determined from prospective studies, but CRLF2 expression is associated with a poor prognosis.
  • Despite their rarity, IGH chromosomal translocations in BCP-ALL therefore define not only new mechanisms of B-cell transformation but also clinically important subgroups of disease and suggest new targeted therapeutic approaches.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Transformation, Neoplastic / metabolism. Immunoglobulin Heavy Chains / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Quantitative Trait Loci. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Animals. Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Leukemic / genetics. Hematopoiesis / genetics. Humans. Inhibitor of Differentiation Proteins / biosynthesis. Inhibitor of Differentiation Proteins / genetics. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Prognosis. Receptors, Cytokine / biosynthesis. Receptors, Cytokine / genetics. Receptors, Erythropoietin / biosynthesis. Receptors, Erythropoietin / genetics

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  • (PMID = 20042721.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRLF2 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / ID4 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / Inhibitor of Differentiation Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Cytokine; 0 / Receptors, Erythropoietin; 0 / TEL-AML1 fusion protein
  • [Number-of-references] 87
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40. Rice R, Guinto P, Dowell-Martino C, He H, Hoyer K, Krenz M, Robbins J, Ingwall JS, Tardiff JC: Cardiac myosin heavy chain isoform exchange alters the phenotype of cTnT-related cardiomyopathies in mouse hearts. J Mol Cell Cardiol; 2010 May;48(5):979-88
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  • [Title] Cardiac myosin heavy chain isoform exchange alters the phenotype of cTnT-related cardiomyopathies in mouse hearts.
  • Familial hypertrophic cardiomyopathy, FHC, is a clinically heterogeneous, autosomal-dominant disease of the cardiac sarcomere leading to extensive remodeling at both the whole heart and molecular levels.
  • The remodeling patterns are mutation-specific, a finding that extends to the level of single amino acid substitutions at the same peptide residue.
  • To determine if a greater economy of contraction at the crossbridge level would rescue the mechanical defects caused by the R92 cTnT mutations, we replaced the endogenous murine alpha-myosin heavy chain (MyHC) with the beta-MyHC isoform.

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
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  • (PMID = 20004663.001).
  • [ISSN] 1095-8584
  • [Journal-full-title] Journal of molecular and cellular cardiology
  • [ISO-abbreviation] J. Mol. Cell. Cardiol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL075619-06; United States / NHLBI NIH HHS / HL / R01-HL-075619-06; United States / NHLBI NIH HHS / HL / F31 HL085915; United States / NHLBI NIH HHS / HL / 5F31-HL-085915-04; United States / NHLBI NIH HHS / HL / R01 HL075619-06; United States / NHLBI NIH HHS / HL / R01 HL075619; United States / NHLBI NIH HHS / HL / R01 HL107046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Troponin T; EC 3.6.4.1 / Myosin Heavy Chains; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ NIHMS164849; NLM/ PMC3016872
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41. Hifumi E, Higashi K, Uda T: Catalytic digestion of human tumor necrosis factor-α by antibody heavy chain. FEBS J; 2010 Sep;277(18):3823-32
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  • [Title] Catalytic digestion of human tumor necrosis factor-α by antibody heavy chain.
  • Tumor necrosis factor-α (TNF-α) is a cytokine and an important molecule concerned with autoimmune diseases such as rheumatoid arthritis, chronic obstructive pulmonary disease, and Crohn's disease.
  • The heavy chain (ETNF-6-H) of the mAb was considered to possess a catalytic triad-like structure in the complementarity determining regions (CDRs).
  • The heavy chain possessed a protease activity against TNF-α with a multicleavage site.
  • [MeSH-major] Antibodies, Catalytic / metabolism. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / metabolism. Immunoglobulin Heavy Chains / metabolism. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] © 2010 The Authors Journal compilation © 2010 FEBS.
  • (PMID = 20718866.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Catalytic; 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Heavy Chains; 0 / Peptides; 0 / Tumor Necrosis Factor-alpha
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42. Haddad F, Qin AX, Bodell PW, Jiang W, Giger JM, Baldwin KM: Intergenic transcription and developmental regulation of cardiac myosin heavy chain genes. Am J Physiol Heart Circ Physiol; 2008 Jan;294(1):H29-40
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  • [Title] Intergenic transcription and developmental regulation of cardiac myosin heavy chain genes.
  • Cardiac myosin heavy chain (MHC) gene expression undergoes a rapid transition from beta- to alpha-MHC during early rodent neonatal development (0-21 days of age).
  • We analyzed the expression of alpha- and beta-MHC at protein, mRNA, and pre-mRNA levels at birth and 7, 10, 15, and 21 days after birth in euthyroid and hypothyroid rodents.
  • On the second half of the IG region, sense transcription occurs, resulting in expression of a sense IG RNA that merges with the alpha-MHC pre-mRNA.
  • This sense IG RNA transcription was detected in the alpha-MHC gene promoter, approximately -1.8 kb relative to the alpha-MHC transcription start site.
  • [MeSH-major] DNA, Intergenic. Gene Expression Regulation, Developmental. Hypothyroidism / genetics. Myocardium / metabolism. Myosin Heavy Chains / genetics. Transcription, Genetic. Ventricular Myosins / genetics
  • [MeSH-minor] Aging. Animals. Animals, Newborn. Base Sequence. Body Weight. Disease Models, Animal. Epigenesis, Genetic. Gene Transfer Techniques. Genes, Reporter. Heart Ventricles / growth & development. Heart Ventricles / metabolism. Molecular Sequence Data. Promoter Regions, Genetic. Propylthiouracil. RNA, Antisense / metabolism. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Transcription Initiation Site. Triiodothyronine / blood

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  • [CommentIn] Am J Physiol Heart Circ Physiol. 2008 Jan;294(1):H14-5 [17993592.001]
  • (PMID = 17982008.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL 073473-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bmyo protein, rat; 0 / DNA, Intergenic; 0 / RNA, Antisense; 0 / RNA, Messenger; 06LU7C9H1V / Triiodothyronine; 721M9407IY / Propylthiouracil; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
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43. Freire G, Ocampo C, Ilbawi N, Griffin AJ, Gupta M: Overt expression of AP-1 reduces alpha myosin heavy chain expression and contributes to heart failure from chronic volume overload. J Mol Cell Cardiol; 2007 Oct;43(4):465-78
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  • [Title] Overt expression of AP-1 reduces alpha myosin heavy chain expression and contributes to heart failure from chronic volume overload.
  • Reduced expression of alpha-MHC plays a significant role in cardiac contractile dysfunction from hemodynamic overload.
  • Previously, Pur proteins and YY1 have been shown to play a role in alpha-MHC repression during heart failure induced by pressure overload and by spontaneous hypertension, respectively.
  • This was not observed in volume-overload-induced heart failure, suggesting additional regulatory mechanisms for alpha-MHC repression.
  • The present study was performed to identify volume overload responsive transcription factors involved in alpha-MHC gene regulation.
  • After 10 weeks of shunt, severe LV dilatation and reduced LV function were accompanied by increased expression of ANF and beta-MHC, and decreased expression of alpha-MHC.
  • In cultured cardiomyocytes, induction of AP-1 by PMA attenuated alpha-MHC mRNA by 60%.
  • Transient transfection assays mapped PMA responsive sequence to -582 to -588 bp of alpha-MHC promoter.
  • Deletion or mutation of these nucleotides had minimal effect on basal promoter activity but played a dominant role in PMA-mediated repression of alpha-MHC promoter activity.
  • Over-expression of c-fos and c-jun in cardiomyocytes inhibited alpha-MHC promoter activity in a concentration dependent manner.
  • Data suggest a repressive role of AP-1 in alpha-MHC expression and its possible involvement in the transition from compensatory hypertrophy to heart failure in chronic volume overload.
  • [MeSH-minor] Animals. Body Weight. Chronic Disease. Gene Expression Profiling. Gene Expression Regulation / physiology. Genes, fos. Genes, jun. Male. Myocardium / pathology. Oligonucleotide Array Sequence Analysis. Organ Size / genetics. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Transcription Factors / genetics. Transcription Factors / physiology. Ventricular Function, Left / genetics

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  • (PMID = 17720185.001).
  • [ISSN] 0022-2828
  • [Journal-full-title] Journal of molecular and cellular cardiology
  • [ISO-abbreviation] J. Mol. Cell. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Transcription Factor AP-1; 0 / Transcription Factors; EC 3.6.1.- / Ventricular Myosins
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44. Korte FS, McDonald KS: Sarcomere length dependence of rat skinned cardiac myocyte mechanical properties: dependence on myosin heavy chain. J Physiol; 2007 Jun 1;581(Pt 2):725-39
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  • [Title] Sarcomere length dependence of rat skinned cardiac myocyte mechanical properties: dependence on myosin heavy chain.
  • The effects of sarcomere length (SL) on sarcomeric loaded shortening velocity, power output and rates of force development were examined in rat skinned cardiac myocytes that contained either alpha-myosin heavy chain (alpha-MyHC) or beta-MyHC at 12 +/- 1 degrees C.
  • When SL was decreased from 2.3 microm to 2.0 microm submaximal isometric force decreased approximately 40% in both alpha-MyHC and beta-MyHC myocytes while peak absolute power output decreased 55% in alpha-MyHC myocytes and 70% in beta-MyHC myocytes.
  • After normalization for the fall in force, peak power output decreased about twice as much in beta-MyHC as in alpha-MyHC myocytes (41% versus 20%).
  • Surprisingly, this led to a 32% greater peak normalized power output at short SL compared to long SL in alpha-MyHC myocytes, whereas in beta-MyHC myocytes peak normalized power output remained depressed at short SL.
  • Addition of 2% dextran at short SL decreased myocyte width and increased force to levels obtained at long SL, and increased peak normalized power output to values greater than at long SL in both alpha-MyHC and beta-MyHC myocytes.
  • The rate constant of force development (k(tr)) was also measured and was not different between long and short SL at the same [Ca(2+)] in alpha-MyHC myocytes but was greater at short SL in beta-MyHC myocytes.
  • At short SL with matched force by either dextran or [Ca(2+)], k(tr) was greater than at long SL in both alpha-MyHC and beta-MyHC myocytes.

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  • (PMID = 17347271.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K02 HL071550; United States / NHLBI NIH HHS / HL / R01 HL057852; United States / NHLBI NIH HHS / HL / K02 HL71550; United States / NHLBI NIH HHS / HL / R01 HL57852
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bmyo protein, rat; 721M9407IY / Propylthiouracil; EC 3.6.4.1 / Myosin Heavy Chains; K3R6ZDH4DU / Dextrans; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2075190
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45. Herron TJ, Devaney E, Mundada L, Arden E, Day S, Guerrero-Serna G, Turner I, Westfall M, Metzger JM: Ca2+-independent positive molecular inotropy for failing rabbit and human cardiac muscle by alpha-myosin motor gene transfer. FASEB J; 2010 Feb;24(2):415-24
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  • [Title] Ca2+-independent positive molecular inotropy for failing rabbit and human cardiac muscle by alpha-myosin motor gene transfer.
  • The purpose of this study was to determine whether fast alpha-myosin molecular motor gene transfer can confer calcium-independent positive inotropy in slow beta-myosin-dominant rabbit and human failing ventricular myocytes.
  • To this end, we generated a recombinant adenovirus (AdMYH6) to deliver the full-length human alpha-myosin gene to adult rabbit and human cardiac myocytes in vitro.
  • Fast alpha-myosin motor expression was determined by Western blotting and immunocytochemical analysis and confocal imaging.
  • Control experiments included the use of a green fluorescent protein or a beta-myosin heavy chain adenovirus.
  • Our data provide evidence for a novel form of calcium-independent positive inotropy in failing cardiac myocytes by fast alpha-myosin motor protein gene transfer.
  • [MeSH-minor] Animals. Cardiac Myosins / genetics. Cloning, Molecular. Disease Models, Animal. Gene Transfer Techniques. Humans. Myocardial Ischemia / physiopathology. Myocardium / metabolism. Myocytes, Cardiac / drug effects. Myocytes, Cardiac / physiology. Myosin Heavy Chains / genetics. Rabbits. Stimulation, Chemical

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  • (PMID = 19801488.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / F32 HL080880; United States / NHLBI NIH HHS / HL / L30 HL082192
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MYH6 protein, human; EC 3.6.1.- / Cardiac Myosins; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC4048941
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46. Fiaccavento R, Carotenuto F, Minieri M, Masuelli L, Vecchini A, Bei R, Modesti A, Binaglia L, Fusco A, Bertoli A, Forte G, Carosella L, Di Nardo P: Alpha-linolenic acid-enriched diet prevents myocardial damage and expands longevity in cardiomyopathic hamsters. Am J Pathol; 2006 Dec;169(6):1913-24
MedlinePlus Health Information. consumer health - Cardiomyopathy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-linolenic acid-enriched diet prevents myocardial damage and expands longevity in cardiomyopathic hamsters.
  • Randomized clinical trials have demonstrated that the increased intake of omega-3 polyunsaturated fatty acids significantly reduces the risk of ischemic cardiovascular disease, but no investigations have been performed in hereditary cardiomyopathies with diffusely damaged myocardium.
  • In the present study, delta-sarcoglycan-null cardiomyopathic hamsters were fed from weaning to death with an alpha-linolenic acid (ALA)-enriched versus standard diet.
  • In fact, ALA administration preserved plasmalemma and mitochondrial membrane integrity, thus maintaining proper cell/extracellular matrix contacts and signaling, as well as a normal gene expression profile (myosin heavy chain isoforms, atrial natriuretic peptide, transforming growth factor-beta1) and a limited extension of fibrotic areas within ALA-fed cardiomyopathic hearts.
  • [MeSH-major] Cardiomegaly / diet therapy. Cardiomyopathies / diet therapy. Dietary Fats, Unsaturated / therapeutic use. Fatty Acids, Omega-3 / therapeutic use. alpha-Linolenic Acid / therapeutic use
  • [MeSH-minor] Animals. Cricetinae. Disease Models, Animal. Endomyocardial Fibrosis / pathology. Endomyocardial Fibrosis / prevention & control. Fatty Acids / blood. Longevity. Myocardial Contraction

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  • (PMID = 17148657.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats, Unsaturated; 0 / Fatty Acids; 0 / Fatty Acids, Omega-3; 0RBV727H71 / alpha-Linolenic Acid
  • [Other-IDs] NLM/ PMC1762468
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47. Hinken AC, McDonald KS: Beta-myosin heavy chain myocytes are more resistant to changes in power output induced by ischemic conditions. Am J Physiol Heart Circ Physiol; 2006 Feb;290(2):H869-77
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  • [Title] Beta-myosin heavy chain myocytes are more resistant to changes in power output induced by ischemic conditions.
  • Also, changes in myosin heavy chain (MHC) isoform toward beta-MHC have been reported after ischemia and infarction associated with coronary artery disease.
  • The purpose of this study was to investigate the effects of myoplasmic changes of P(i) and H+ on the loaded shortening velocity and power output of cardiac myocytes expressing either alpha- or beta-MHC.
  • Added P(i) and lowered pH each caused isometric force to decline to the same extent in alpha-MHC and beta-MHC myocytes; however, beta-MHC myocytes were more resistant to changes in absolute power output.
  • For example, peak absolute power output fell 53% in alpha-MHC myocytes, whereas power fell only 38% in beta-MHC myocytes in response to elevated P(i) and lowered pH (i.e., solution 4).
  • [MeSH-major] Energy Metabolism. Muscle Contraction. Myocardial Ischemia / physiopathology. Myocytes, Cardiac / metabolism. Myosin Heavy Chains / metabolism

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  • (PMID = 16172167.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / K01-HL-71550; United States / NHLBI NIH HHS / HL / R01-HL-57852
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites; 0 / Bmyo protein, rat; 0 / Phosphates; 721M9407IY / Propylthiouracil; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
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48. Kogelberg H, Tolner B, Thomas GJ, Di Cara D, Minogue S, Ramesh B, Sodha S, Marsh D, Lowdell MW, Meyer T, Begent RH, Hart I, Marshall JF, Chester K: Engineering a single-chain Fv antibody to alpha v beta 6 integrin using the specificity-determining loop of a foot-and-mouth disease virus. J Mol Biol; 2008 Oct 03;382(2):385-401
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  • [Title] Engineering a single-chain Fv antibody to alpha v beta 6 integrin using the specificity-determining loop of a foot-and-mouth disease virus.
  • The alpha v beta 6 integrin is a promising target for cancer therapy.
  • Its expression is up-regulated de novo on many types of carcinoma where it may activate transforming growth factor-beta1 and transforming growth factor-beta 3, interact with the specific extracellular matrix proteins and promote migration and invasion of tumor cells.
  • The viral protein 1 (VP1) coat protein of the O(1) British field strain serotype of foot-and-mouth disease virus is a high-affinity ligand for alpha v beta 6, and we recently reported that a peptide derived from VP1 exhibited alpha v beta 6-specific binding in vitro and in vivo.
  • We hypothesized that this peptide could confer binding specificity of an antibody to alpha v beta 6.
  • A 17-mer peptide of VP1 was inserted into the complementarity-determining region H3 loop of MFE-23, a murine single-chain Fv (scFv) antibody reactive with carcinoembryonic antigen (CEA).
  • The resultant scFv (B6-1) bound to alpha v beta 6 but retained residual reactivity with CEA.
  • This was eliminated by point mutation (Y100bP) in the variable heavy-chain domain to create an scFv (B6-2) that was as structurally stable as MFE-23 and reacted specifically with alpha v beta 6 but not with alpha 5 beta 1, alpha v beta 3, alpha v beta 5, alpha v beta 8 or CEA.
  • B6-2 was internalized into alpha v beta 6-expressing cells and inhibited alpha v beta 6-dependent migration of carcinoma cells.
  • The humanized form (B6-3) was obtained as a non-covalent dimer from secretion in Pichia pastoris (115 mg/l) and was a potent inhibitor of alpha v beta 6-mediated cell adhesion.
  • Thus, we have used a rational stepwise approach to create a humanized scFv with therapeutic potential to block alpha v beta 6-mediated cancer cell invasion or to deliver and internalize toxins specifically to alpha v beta 6-expressing tumors.
  • [MeSH-minor] Amino Acid Sequence. Animals. Capsid Proteins / chemistry. Capsid Proteins / genetics. Capsid Proteins / immunology. Carcinoembryonic Antigen / chemistry. Carcinoembryonic Antigen / genetics. Cell Line. Cell Movement. Foot-and-Mouth Disease Virus. Humans. Mice. Models, Molecular. Molecular Sequence Data. Oligopeptides / chemistry. Oligopeptides / genetics. Protein Conformation

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  • (PMID = 18656482.001).
  • [ISSN] 1089-8638
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A5149; United Kingdom / Cancer Research UK / / C34/A5149
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Capsid Proteins; 0 / Carcinoembryonic Antigen; 0 / Complementarity Determining Regions; 0 / Immunoglobulin Fragments; 0 / Immunoglobulin Variable Region; 0 / Integrins; 0 / Oligopeptides; 0 / VP1 protein, Foot-and-mouth disease virus; 0 / integrin alphavbeta6; 78VO7F77PN / arginyl-glycyl-aspartic acid
  • [Other-IDs] NLM/ PMC2958364; NLM/ UKMS2297
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49. Budde BS, Binner P, Waldmüller S, Höhne W, Blankenfeldt W, Hassfeld S, Brömsen J, Dermintzoglou A, Wieczorek M, May E, Kirst E, Selignow C, Rackebrandt K, Müller M, Goody RS, Vosberg HP, Nürnberg P, Scheffold T: Noncompaction of the ventricular myocardium is associated with a de novo mutation in the beta-myosin heavy chain gene. PLoS One; 2007;2(12):e1362

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Noncompaction of the ventricular myocardium is associated with a de novo mutation in the beta-myosin heavy chain gene.
  • Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin.
  • For molecular characterization, a genome-wide linkage analysis was undertaken and the disease locus was mapped to chromosome 14ptel-14q12.
  • Subsequently, two genes of the disease interval, MYH6 and MYH7 (encoding the alpha- and beta-myosin heavy chain, respectively) were sequenced, leading to the identification of a previously unknown de novo missense mutation, c.842G>C, in the gene MYH7.
  • A high degree of clinical variability was observed, ranging from the absence of symptoms in childhood to cardiac death in the third decade of life.
  • [MeSH-major] Heart Ventricles / metabolism. Mutation, Missense. Myosin Heavy Chains / genetics

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  • (PMID = 18159245.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ PMC2137931
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50. Chen SE, Jin B, Li YP: TNF-alpha regulates myogenesis and muscle regeneration by activating p38 MAPK. Am J Physiol Cell Physiol; 2007 May;292(5):C1660-71
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TNF-alpha regulates myogenesis and muscle regeneration by activating p38 MAPK.
  • We recently reported that p38 activation, myogenesis, and regeneration in cardiotoxin-injured soleus muscle are impaired in TNF-alpha receptor double-knockout (p55(-/-)p75(-/-)) mice.
  • To fully evaluate the role of TNF-alpha in myogenic activation of p38, we tried to determine whether p38 activation in differentiating myoblasts requires autocrine TNF-alpha, and whether forced activation of p38 rescues impaired myogenesis and regeneration in the p55(-/-)p75(-/-) soleus.
  • We observed an increase of TNF-alpha release from C2C12 or mouse primary myoblasts placed in low-serum differentiation medium.
  • A TNF-alpha-neutralizing antibody added to differentiation medium blocked p38 activation and suppressed differentiation markers myocyte enhancer factor (MEF)-2C, myogenin, p21, and myosin heavy chain in C2C12 myoblasts.
  • Conversely, recombinant TNF-alpha added to differentiation medium stimulated myogenesis at 0.05 ng/ml while inhibited it at 0.5 and 5 ng/ml.
  • Increased TNF-alpha release was also seen in cardiotoxin-injured soleus over the course of regeneration.
  • These results indicate that TNF-alpha regulates myogenesis and muscle regeneration as a key activator of p38.

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  • (PMID = 17151142.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / AR049022-04; United States / NIAMS NIH HHS / AR / R01 AR049022; United States / NIAMS NIH HHS / AR / AR-049022; United States / NIAMS NIH HHS / AR / R01 AR049022-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cobra Cardiotoxin Proteins; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 6
  • [Other-IDs] NLM/ NIHMS226377; NLM/ PMC3099536
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51. North KN, Laing NG: Skeletal muscle alpha-actin diseases. Adv Exp Med Biol; 2008;642:15-27
FlyBase. FlyBase .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Skeletal muscle alpha-actin diseases.
  • Skeletal muscle alpha-actin is the principal protein component of the adult skeletal muscle thin filament.
  • The interaction between skeletal muscle alpha-actin and the various myosin heavy chain proteins in the different muscle fibre types generates the force of muscle contraction.
  • Skeletal muscle alpha-alpha actin is thus of fundamental importance to normal muscle contraction.
  • To date over 140 different disease-causing mutations have been identified in the skeletal muscle alpha-actin gene ACTA1.
  • These mutations are associated with histologically distinct congenital myopathies, including nemaline myopathy, actin myopathy, intranuclear rod myopathy, congenital fibre type disproportion and myopathy with cores.
  • Mutations in ACTA1 are associated with a wide range of clinical severity although the majority of patients tend to have severe congenital-onset disease.
  • Most of the patients have de novo dominant mutations not present in either parent.
  • However mild ACTA1 disease may be dominantly inherited and there are also recessive mutations.
  • Information from the clinic suggests that exercise and L-tyrosine may benefit some patients and that in the future decreasing the proportion of mutant actin may ameliorate the disease in some patients.
  • [MeSH-major] Actins / metabolism. Muscular Diseases / metabolism

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  • (PMID = 19181090.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins
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52. Kasturirangan S, Brune D, Sierks M: Promoting alpha-secretase cleavage of beta-amyloid with engineered proteolytic antibody fragments. Biotechnol Prog; 2009 Jul-Aug;25(4):1054-63
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoting alpha-secretase cleavage of beta-amyloid with engineered proteolytic antibody fragments.
  • Deposition of beta-amyloid (A beta) is considered as an important early event in the pathogenesis of Alzheimer's Disease (AD), and reduction of A beta levels by various therapeutic approaches is actively being pursued.
  • A potentially non-inflammatory approach to facilitate clearance and reduce toxicity is to hydrolyze A beta at its alpha-secretase site.
  • We have previously identified a light chain fragment, mk18, with alpha-secretase-like catalytic activity, producing the 1-16 and 17-40 amino acid fragments of A beta 40 as primary products, although hydrolysis is also observed following other lysine and arginine residues.
  • To improve the specific activity of the recombinant antibody by affinity maturation, we constructed a single chain variable fragment (scFv) library containing a randomized CDR3 heavy chain region.
  • A biotinylated covalently reactive analog mimicking alpha-secretase site cleavage was synthesized, immobilized on streptavidin beads, and used to select yeast surface expressed scFvs with increased specificity for A beta.
  • After two rounds of selection against the analog, yeast cells were individually screened for proteolytic activity towards an internally quenched fluorogenic substrate that contains the alpha-secretase site of A beta.
  • [MeSH-major] Alzheimer Disease / metabolism. Amyloid Precursor Protein Secretases / metabolism. Amyloid beta-Peptides / metabolism. Immunoglobulin Variable Region / metabolism. Protein Engineering

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  • [Copyright] (c) 2009 American Institute of Chemical Engineers. Biotechnol. Prog., 2009.
  • (PMID = 19572401.001).
  • [ISSN] 1520-6033
  • [Journal-full-title] Biotechnology progress
  • [ISO-abbreviation] Biotechnol. Prog.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Immunoglobulin Variable Region; 0 / Recombinant Proteins; EC 3.4.- / Amyloid Precursor Protein Secretases
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53. Horton MJ, Rosen C, Close JM, Sciote JJ: Quantification of myosin heavy chain RNA in human laryngeal muscles: differential expression in the vertical and horizontal posterior cricoarytenoid and thyroarytenoid. Laryngoscope; 2008 Mar;118(3):472-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantification of myosin heavy chain RNA in human laryngeal muscles: differential expression in the vertical and horizontal posterior cricoarytenoid and thyroarytenoid.
  • BACKGROUND: Human laryngeal muscles are composed of fibers that express type I, IIA, and IIX myosin heavy chains (MyHC), but the presence and quantity of atypical myosins such as perinatal, extraocular, IIB, and alpha (cardiac) remain in question.
  • The distribution of myosin, the main motor protein, in relation to structure-function relationships in this specialized muscle group will be important for understanding laryngeal function in both health and disease.
  • OBJECTIVES: We determined the quantity of MyHC genes expressed in human posterior cricoarytenoid (PCA) and thyroarytenoid (TA) muscle using real-time quantitative reverse-transcriptase polymerase chain reaction in a large number of samples taken from laryngectomy subjects.
  • Low but detectable amounts of perinatal and alpha gene message are present in both of the intrinsic laryngeal muscles.

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  • (PMID = 18091331.001).
  • [ISSN] 0023-852X
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] ENG
  • [Grant] United States / NIDCD NIH HHS / DC / R01 DC005058; United States / PHS HHS / / NIDCD 5058-3
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 63231-63-0 / RNA; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ NIHMS534004; NLM/ PMC3879044
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54. Kim SK, Park IK, Park BH, Park W, Lee HS, Kim TH, Jun JB, Bae SC, Yoo DH, Uhm WS: A case report: isolated a heavy chain monoclonal gammopathy in a patient with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin change syndrome. Int J Clin Pract Suppl; 2005 Apr;(147):26-30
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  • [Title] A case report: isolated a heavy chain monoclonal gammopathy in a patient with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin change syndrome.
  • A 45-year-old South-Korean man presented with abdominal distension, progressive paresthesia and motor weakness of both lower extremities.
  • Circulating M components of POEMS syndrome consist mainly of IgG or IgA-lambda and rarely IgM-lambda, IgG-kappa or isolated light chains.
  • In this case, the M-band on serum protein electrophoresis and isolated IgA heavy chain on serum immunofixation electrophoresis were demonstrated, but there was no abnormal light chain.
  • We suggest that this case may be associated with a pattern of abnormal secretion of monoclonal protein or a coincidence of a heavy chain disease in POEMS syndrome, even though the latter possibility may be very rare.
  • [MeSH-major] Heavy Chain Disease / diagnosis. POEMS Syndrome / diagnosis
  • [MeSH-minor] Bone Marrow / radionuclide imaging. Humans. Immunoglobulin A / blood. Immunoglobulin alpha-Chains / blood. Male. Middle Aged. Pleural Effusion / radiography. Pulmonary Atelectasis / radiography

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  • (PMID = 15875614.001).
  • [ISSN] 1368-504X
  • [Journal-full-title] International journal of clinical practice. Supplement
  • [ISO-abbreviation] Int J Clin Pract Suppl
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin A; 0 / Immunoglobulin alpha-Chains
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55. Vychodilova-Krenkova L, Matiasovic J, Horin P: Single nucleotide polymorphisms in four functionally related immune response genes in the horse: CD14,TLR4, Cepsilon, andFcepsilon R1 alpha. Int J Immunogenet; 2005 Oct;32(5):277-83

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  • [Title] Single nucleotide polymorphisms in four functionally related immune response genes in the horse: CD14,TLR4, Cepsilon, andFcepsilon R1 alpha.
  • The objective of this study was to identify single nucleotide polymorphisms (SNPs) within four functionally related immune response genes in the horse, and to develop genotyping techniques that could be useful for future genomic studies of horse infectious and allergic diseases.
  • The genes analysed were: the lipopolysaccharide (LPS) receptor gene CD14, the toll-like receptor 4 gene TLR4, the gene Cepsilon encoding the IgE heavy chain molecule and the gene FcepsilonR1 alpha coding for the alpha subunit of the IgE receptor molecule.
  • Horse-specific primers amplifying selected gene regions were designed and SNPs were searched by selective resequencing and/or by PCR-SSCP (polymerase chain reaction-sequence specific conformational polymorphism) or PCR-RFLP (PCR-restriction fragment length polymorphism).
  • Three SNPs were found in the CD14 gene, four in the TLR4 gene; two SNPs were identified in the Cepsilon gene, and one SNP was found in the FcepsilonR1 alpha gene.
  • The methods developed for genotyping and haplotyping the SNPs identified represent, along with markers described previously, a potentially useful tool for genomic analysis of the function and role of these genes in immunity and in mechanisms of disease.

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  • (PMID = 16164694.001).
  • [ISSN] 1744-3121
  • [Journal-full-title] International journal of immunogenetics
  • [ISO-abbreviation] Int. J. Immunogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Immunologic
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56. Ching YH, Ghosh TK, Cross SJ, Packham EA, Honeyman L, Loughna S, Robinson TE, Dearlove AM, Ribas G, Bonser AJ, Thomas NR, Scotter AJ, Caves LS, Tyrrell GP, Newbury-Ecob RA, Munnich A, Bonnet D, Brook JD: Mutation in myosin heavy chain 6 causes atrial septal defect. Nat Genet; 2005 Apr;37(4):423-8
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  • [Title] Mutation in myosin heavy chain 6 causes atrial septal defect.
  • The underlying mutation is a missense substitution, I820N, in alpha-myosin heavy chain (MYH6), a structural protein expressed at high levels in the developing atria, which affects the binding of the heavy chain to its regulatory light chain.
  • These data provide evidence for a link between a transcription factor, a structural protein and congenital heart disease.
  • [MeSH-major] Cardiac Myosins / genetics. Heart Septal Defects, Atrial / genetics. Mutation, Missense. Myosin Heavy Chains / genetics. T-Box Domain Proteins / genetics


57. Herron TJ, Vandenboom R, Fomicheva E, Mundada L, Edwards T, Metzger JM: Calcium-independent negative inotropy by beta-myosin heavy chain gene transfer in cardiac myocytes. Circ Res; 2007 Apr 27;100(8):1182-90
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  • [Title] Calcium-independent negative inotropy by beta-myosin heavy chain gene transfer in cardiac myocytes.
  • Increased relative expression of the slow molecular motor of the heart (beta-myosin heavy chain [MyHC]) is well known to occur in many rodent models of cardiovascular disease and in human heart failure.
  • To determine the direct effects of increased relative beta-MyHC expression on cardiac contractility, we used acute genetic engineering with a recombinant adenoviral vector (AdMYH7) to genetically titrate beta-MyHC protein expression in isolated rodent ventricular cardiac myocytes that predominantly expressed alpha-MyHC (fast molecular motor).
  • Gene transfer-based replacement of alpha-MyHC with beta-MyHC attenuated contractility in a dose-dependent manner, whereas calcium transients were unaffected.
  • Results indicate that small increases of beta-MyHC expression (18%) have Ca2+ transient-independent physiologically relevant effects to decrease intact cardiac myocyte function.

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  • (PMID = 17363698.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL60048; United States / NHLBI NIH HHS / HL / F32 HL080880; United States / NHLBI NIH HHS / HL / L30 HL082192; United States / NHLBI NIH HHS / HL / HL080880; United States / NIDDK NIH HHS / DK / 5P60 DK20572
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bmyo protein, rat; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains; SY7Q814VUP / Calcium
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58. Strle K, Broussard SR, McCusker RH, Shen WH, LeCleir JM, Johnson RW, Freund GG, Dantzer R, Kelley KW: C-jun N-terminal kinase mediates tumor necrosis factor-alpha suppression of differentiation in myoblasts. Endocrinology; 2006 Sep;147(9):4363-73
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  • [Title] C-jun N-terminal kinase mediates tumor necrosis factor-alpha suppression of differentiation in myoblasts.
  • The stress kinase c-jun N-terminal kinase (JNK) was recently shown to be involved in the pathophysiology of major inflammatory conditions, including Alzheimer's disease, stroke, obesity, and type II diabetes.
  • More importantly, JNK activation induced by TNFalpha, C2-ceramide, and N-SMase is associated with reduced expression of the critical muscle transcription factor myogenin as well as the differentiation marker myosin heavy chain (MHC).
  • [MeSH-major] Cell Differentiation / drug effects. JNK Mitogen-Activated Protein Kinases / physiology. Myoblasts / cytology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Anisomycin / pharmacology. Cell Line. Enzyme Activation / drug effects. Enzyme Inhibitors / pharmacology. Gene Expression / drug effects. Humans. Inflammation. Insulin Receptor Substrate Proteins. Insulin-Like Growth Factor I / antagonists & inhibitors. Insulin-Like Growth Factor I / pharmacology. Insulin-Like Growth Factor I / physiology. Kinetics. Mice. Myogenin / antagonists & inhibitors. Myogenin / genetics. Phosphoproteins / metabolism. Phosphorylation. Receptor, IGF Type 1 / antagonists & inhibitors. Receptor, IGF Type 1 / metabolism. Recombinant Proteins. Signal Transduction / drug effects. Sphingomyelin Phosphodiesterase / pharmacology. Sphingosine / analogs & derivatives. Sphingosine / pharmacology. Tyrosine / metabolism

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  • (PMID = 16777978.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG023580; United States / NIA NIH HHS / AG / AG16710; United States / NIAID NIH HHS / AI / AI50442; United States / NIDDK NIH HHS / DK / DK064862; United States / NIMH NIH HHS / MH / MH071349; United States / NIMH NIH HHS / MH / MH51569
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / IRS1 protein, human; 0 / Insulin Receptor Substrate Proteins; 0 / Irs1 protein, mouse; 0 / Myogenin; 0 / N-acetylsphingosine; 0 / Phosphoproteins; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 42HK56048U / Tyrosine; 67763-96-6 / Insulin-Like Growth Factor I; 6C74YM2NGI / Anisomycin; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.1.4.12 / Sphingomyelin Phosphodiesterase; NGZ37HRE42 / Sphingosine
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59. Paessler S, Yun NE, Judy BM, Dziuba N, Zacks MA, Grund AH, Frolov I, Campbell GA, Weaver SC, Estes DM: Alpha-beta T cells provide protection against lethal encephalitis in the murine model of VEEV infection. Virology; 2007 Oct 25;367(2):307-23
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  • [Title] Alpha-beta T cells provide protection against lethal encephalitis in the murine model of VEEV infection.
  • Wild type mice were protected against lethal VEEV challenge.
  • In contrast, alpha/beta (alphabeta) TCR-deficient mice developed lethal encephalitis following VEEV challenge, while mice deficient in gamma/delta (gammadelta) T cells were protected.
  • Surprisingly, the vaccine potency was diminished by 50% in animals lacking interferon-gamma receptor alpha chain (R1)-chain and a minority of vaccinated immunoglobulin heavy chain-deficient (microMT) mice survived challenge, which suggests that neutralizing antibody may not be absolutely required for protection.

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  • (PMID = 17610927.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / K08 AI059491; United States / NIAID NIH HHS / AI / U54 AI057156; United States / NIAID NIH HHS / AI / K08 AI059491-01; United States / NIAID NIH HHS / AI / AI059491-01; None / None / / U54 AI057156-05; United States / NIAID NIH HHS / AI / K08 AI059491-04; United States / NIAID NIH HHS / AI / AI059491-02; United States / NIAID NIH HHS / AI / K08 AI059491-03; United States / NIAID NIH HHS / AI / AI059491-03; United States / NIAID NIH HHS / AI / K08 AI059491-02; United States / NIAID NIH HHS / AI / U54 AI057156-05; United States / NIAID NIH HHS / AI / AI059491-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Vaccines, Attenuated; 0 / Viral Vaccines
  • [Other-IDs] NLM/ NIHMS32492; NLM/ PMC2067255
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60. Remels AH, Gosker HR, Schrauwen P, Hommelberg PP, Sliwinski P, Polkey M, Galdiz J, Wouters EF, Langen RC, Schols AM: TNF-alpha impairs regulation of muscle oxidative phenotype: implications for cachexia? FASEB J; 2010 Dec;24(12):5052-62
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  • [Title] TNF-alpha impairs regulation of muscle oxidative phenotype: implications for cachexia?
  • Chronic obstructive pulmonary disease (COPD) is characterized by weight loss, muscle wasting (in advanced disease ultimately resulting in cachexia), and loss of muscle oxidative phenotype (oxphen).
  • In cultured muscle cells, mitochondrial protein content and myosin heavy chain isoform I (but not II) protein and mRNA levels were reduced on chronic TNF-α stimulation.
  • [MeSH-major] Cachexia / metabolism. Muscle, Skeletal / metabolism. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Blotting, Western. Cell Line. Citrate (si)-Synthase / metabolism. DNA-Binding Proteins / metabolism. Electron Transport Complex IV / metabolism. Electrophoretic Mobility Shift Assay. Enzyme-Linked Immunosorbent Assay. Heat-Shock Proteins / metabolism. Humans. Hydro-Lyases / metabolism. Mice. Mitochondrial Proteins / metabolism. NF-kappa B / genetics. NF-kappa B / metabolism. PPAR alpha / metabolism. Pulmonary Disease, Chronic Obstructive / metabolism. Transcription Factors / metabolism

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  • (PMID = 20807714.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Heat-Shock Proteins; 0 / Mitochondrial Proteins; 0 / NF-kappa B; 0 / PPAR alpha; 0 / PPARGC1A protein, human; 0 / TFAM protein, human; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; EC 1.9.3.1 / Electron Transport Complex IV; EC 2.3.3.1 / Citrate (si)-Synthase; EC 4.2.1.- / D-3-hydroxyacyl CoA dehydratase; EC 4.2.1.- / Hydro-Lyases
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61. Liao PC, Yu L, Kuo CC, Lin C, Kuo YM: Proteomics analysis of plasma for potential biomarkers in the diagnosis of Alzheimer's disease. Proteomics Clin Appl; 2007 May;1(5):506-12
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  • [Title] Proteomics analysis of plasma for potential biomarkers in the diagnosis of Alzheimer's disease.
  • The objective of this study was to search for biological markers associated with Alzheimer's disease (AD).
  • Plasma specimens obtained from ten pathologically diagnosed AD patients and ten non-demented (ND) control subjects were analyzed by a combination of 2-DE and MS.
  • This strategy allowed us to identify six plasma proteins (alpha-1-antitrypsin, vitamin D-binding protein, inter-alpha-trypsin inhibitor family heavy chain-related protein, apolipoprotein J precursor, cAMP-dependent protein kinase catalytic subunit alpha 1, and an orf) whose 2-DE spot densities were different between the AD and ND groups.
  • Due to their involvements in AD amyloid plaque formation, the plasma concentrations of alpha-1-antitrypsin and apolipoprotein J were further validated using either ELISA or Western blot.
  • The results revealed that the plasma levels of alpha-1-antitrypsin in AD were higher than those of controls, confirming the 2-DE findings.
  • Considering the difference in resolving power to differentially quantitate protein isoforms provided by 2-DE and Western blot, 2-DE analysis combined with MS protein identification offers distinctive advantages when a disease-related protein isoform-specific variance is investigated.

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  • [Copyright] Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21136702.001).
  • [ISSN] 1862-8346
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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62. Sun B, Young SP, Li P, Di C, Brown T, Salva MZ, Li S, Bird A, Yan Z, Auten R, Hauschka SD, Koeberl DD: Correction of multiple striated muscles in murine Pompe disease through adeno-associated virus-mediated gene therapy. Mol Ther; 2008 Aug;16(8):1366-71
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  • [Title] Correction of multiple striated muscles in murine Pompe disease through adeno-associated virus-mediated gene therapy.
  • Glycogen storage disease type II (Pompe disease; MIM 232300) stems from the deficiency of acid alpha-glucosidase (GAA; acid maltase; EC 3.2.1.20), which primarily involves cardiac and skeletal muscles.
  • An adeno-associated virus 2/8 (AAV2/8) vector containing the muscle creatine kinase (MCK) (CK1) reduced glycogen content by approximately 50% in the heart and quadriceps in GAA-knockout (GAA-KO) mice; furthermore, an AAV2/8 vector containing the hybrid alpha-myosin heavy chain enhancer-/MCK enhancer-promoter (MHCK7) cassette reduced glycogen content by >95% in heart and >75% in the diaphragm and quadriceps.
  • Importantly, type IIb myofibers in the extensor digitalis longus (EDL) were transduced, thereby correcting a myofiber type that is unresponsive to enzyme replacement therapy.
  • In summary, AAV8 and AAV9-pseudotyped vectors containing the MHCK7 regulatory cassette achieved enhanced efficacy in Pompe disease mice.
  • [MeSH-major] Dependovirus / genetics. Genetic Therapy / methods. Glycogen Storage Disease Type II / therapy. Muscle, Striated / metabolism
  • [MeSH-minor] Animals. Creatine Kinase, MM Form / genetics. Creatine Kinase, MM Form / metabolism. Enhancer Elements, Genetic / genetics. Female. Genetic Vectors / genetics. Glycogen / metabolism. Hindlimb / metabolism. Hindlimb / pathology. Mice. Mice, Knockout. Muscle, Skeletal / metabolism. Muscle, Skeletal / pathology. Myocardium / metabolism. Myosin Heavy Chains / genetics. Promoter Regions, Genetic / genetics. Quadriceps Muscle / metabolism. Quadriceps Muscle / pathology. Transduction, Genetic. alpha-Glucosidases / genetics. alpha-Glucosidases / metabolism

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  • (PMID = 18560415.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL081122; United States / NHLBI NIH HHS / HL / R01 HL081122-01A1; United States / NIAMS NIH HHS / AR / R01 AR18860; United States / NHLBI NIH HHS / HL / R01 HL081122-03; United States / NICHD NIH HHS / HD / 1 U54 HD047175; United States / NICHD NIH HHS / HD / U54 HD047175; United States / NHLBI NIH HHS / HL / R24 HL064387; United States / NIAMS NIH HHS / AR / R01 AR018860; United States / NHLBI NIH HHS / HL / R01 HL081122-02; United States / NHLBI NIH HHS / HL / R24 HL64387
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9005-79-2 / Glycogen; EC 2.7.3.2 / Creatine Kinase, MM Form; EC 3.2.1.20 / alpha-Glucosidases; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ NIHMS107993; NLM/ PMC2670546
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63. de Frutos S, Spangler R, Alò D, Bosc LV: NFATc3 mediates chronic hypoxia-induced pulmonary arterial remodeling with alpha-actin up-regulation. J Biol Chem; 2007 May 18;282(20):15081-9
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  • [Title] NFATc3 mediates chronic hypoxia-induced pulmonary arterial remodeling with alpha-actin up-regulation.
  • During pulmonary hypertension, pulmonary arteries exhibit increased expression of smooth muscle-alpha-actin and -myosin heavy chain.
  • NFATc3 (nuclear factor of activated T cells isoform c3), which is aCa(2+)-dependent transcription factor, has been recently linked to smooth muscle phenotypic maintenance through the regulation of the expression of alpha-actin.
  • The aim of this study was to determine if: (a) NFATc3 is expressed in murine pulmonary arteries, (b) hypoxia induces NFAT activation, (c) NFATc3 mediates the up-regulation of alpha-actin during chronic hypoxia, and (d) NFATc3 is involved in chronic hypoxia-induced pulmonary vascular remodeling.
  • Hypoxia induced up-regulation of alpha-actin and was prevented by the calcineurin/NFAT inhibitor, cyclosporin A (25 mg/kg/day s.c.).
  • In addition, NFATc3 knock-out mice did not showed increased alpha-actin levels and arterial wall thickness after hypoxia.

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  • (PMID = 17403661.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL088151-01A1; United States / NHLBI NIH HHS / HL / R01 HL088151; United States / NHLBI NIH HHS / HL / R01 HL088151-01A1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Calcineurin Inhibitors; 0 / Enzyme Inhibitors; 0 / NFATC Transcription Factors; 0 / Nfatc3 protein, mouse; 83HN0GTJ6D / Cyclosporine; EC 3.1.3.16 / Calcineurin
  • [Other-IDs] NLM/ NIHMS64231; NLM/ PMC2754407
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64. Shaye OS, Levine AM: Marginal zone lymphoma. J Natl Compr Canc Netw; 2006 Mar;4(3):311-8
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  • [Title] Marginal zone lymphoma.
  • Marginal zone lymphomas (MZLs) comprise 3 distinct entities: extranodal MZL of mucosa-associated lymphoid tissue (MALT), splenic MZL, and nodal MZL.
  • Gastric MALT lymphoma is the most common extranodal MZL and often develops as a result of chronic Helicobacter pylori gastritis.
  • Antigen-driven lymphomatous disease can also be seen in the association of Borrelia burgdorferi with MALT lymphoma of the skin, Chlamydia psittaci with MALT lymphoma of the ocular adnexa, Campylobacter jejuni with immunoproliferative disease of the small intestine, and hepatitis C with splenic MZL.
  • This article discusses the pathogenesis and clinical features of MZL and the treatment options available to patients.
  • [MeSH-major] Helicobacter Infections / complications. Lymphoma / diagnosis. Lymphoma / therapy. Splenic Neoplasms. Stomach Neoplasms
  • [MeSH-minor] Chronic Disease. Gastritis / microbiology. Helicobacter pylori. Humans. Lymphoma, B-Cell, Marginal Zone

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  • (PMID = 16507274.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 73
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65. Guo DC, Pannu H, Tran-Fadulu V, Papke CL, Yu RK, Avidan N, Bourgeois S, Estrera AL, Safi HJ, Sparks E, Amor D, Ades L, McConnell V, Willoughby CE, Abuelo D, Willing M, Lewis RA, Kim DH, Scherer S, Tung PP, Ahn C, Buja LM, Raman CS, Shete SS, Milewicz DM: Mutations in smooth muscle alpha-actin (ACTA2) lead to thoracic aortic aneurysms and dissections. Nat Genet; 2007 Dec;39(12):1488-93
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  • [Title] Mutations in smooth muscle alpha-actin (ACTA2) lead to thoracic aortic aneurysms and dissections.
  • SMC contractile force requires cyclic interactions between SMC alpha-actin (encoded by ACTA2) and the beta-myosin heavy chain (encoded by MYH11).
  • [MeSH-minor] Aorta / metabolism. Aorta / pathology. Female. Genetic Predisposition to Disease. Humans. Male. Myocytes, Smooth Muscle / metabolism. Myocytes, Smooth Muscle / pathology. Pedigree


66. Mahimkar R, Nguyen A, Mann M, Yeh CC, Zhu BQ, Karliner JS, Lovett DH: Cardiac transgenic matrix metalloproteinase-2 expression induces myxomatous valve degeneration: a potential model of mitral valve prolapse disease. Cardiovasc Pathol; 2009 Sep-Oct;18(5):253-61
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  • [Title] Cardiac transgenic matrix metalloproteinase-2 expression induces myxomatous valve degeneration: a potential model of mitral valve prolapse disease.
  • INTRODUCTION: Myxomatous mitral valve "degeneration" with prolapse (MVP) is the most frequent form of nonischemic mitral valve disease.
  • METHODS: We generated mice with cardiac-specific expression of constitutively active MMP-2 under the control of the alpha-myosin heavy chain promoter.
  • The cardiac-specific MMP-2 transgenic mouse potentially provides a unique experimental platform for the evaluation of nonsurgical therapies based on the underlying pathophysiology of this disease.

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  • (PMID = 18835790.001).
  • [ISSN] 1879-1336
  • [Journal-full-title] Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
  • [ISO-abbreviation] Cardiovasc. Pathol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL068738-05; United States / NHLBI NIH HHS / HL / HL068738-05; United States / NHLBI NIH HHS / HL / R01 HL090606; United States / NHLBI NIH HHS / HL / P01 HL068738; United States / NHLBI NIH HHS / HL / P01-HL-68738
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ NIHMS380615; NLM/ PMC3367668
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67. Kido M, Du L, Sullivan CC, Li X, Deutsch R, Jamieson SW, Thistlethwaite PA: Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunction after myocardial infarction in the mouse. J Am Coll Cardiol; 2005 Dec 6;46(11):2116-24
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  • [Title] Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunction after myocardial infarction in the mouse.
  • OBJECTIVES: The aim of this research was to test whether constitutive expression of hypoxia-inducible factor 1-alpha (HIF-1alpha) influences infarction size and cardiac performance after myocardial infarction.
  • BACKGROUND: A major question in clinical medicine is whether infarction size and border zone remodeling of the heart can be influenced by the overexpression of specific genes in the peri-infarction region.
  • Transgenic mice containing the HIF-1alpha gene under the control of the alpha-myosin heavy chain promoter were constructed.
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Disease Progression. Immunohistochemistry. Male. Mice. Mice, Transgenic. Neovascularization, Physiologic / physiology. Nitric Oxide Synthase Type II / metabolism. Transcription, Genetic / physiology. Vascular Endothelial Growth Factor A / metabolism. Ventricular Function, Left. Ventricular Remodeling / physiology

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  • (PMID = 16325051.001).
  • [ISSN] 1558-3597
  • [Journal-full-title] Journal of the American College of Cardiology
  • [ISO-abbreviation] J. Am. Coll. Cardiol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR00827; United States / NHLBI NIH HHS / HL / R01 HL70852
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1; 0 / Vascular Endothelial Growth Factor A; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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68. Baptista MJ, Recamán M, Melo-Rocha G, Nogueira-Silva C, Roriz JM, Soares-Fernandes J, Gonzaga S, Santos M, Leite-Moreira A, Areias JC, Correia-Pinto J: Myocardium expression of connexin 43, SERCA2a, and myosin heavy chain isoforms are preserved in nitrofen-induced congenital diaphragmatic hernia rat model. J Pediatr Surg; 2006 Sep;41(9):1532-8
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  • [Title] Myocardium expression of connexin 43, SERCA2a, and myosin heavy chain isoforms are preserved in nitrofen-induced congenital diaphragmatic hernia rat model.
  • Myocardium maturation is associated with age-dependent increasing of gene expression of gap junction protein connexin 43 (Cx43), adenosine triphosphatase of the sarcoplasmic reticulum (SERCA2a), as well as switching of myosin heavy chains (MHCs) from beta to alpha isoforms.
  • Myocardial samples collected from left ventricle free wall were processed to (i) quantification of messenger RNA (mRNA) of Cx43, SERCA2a, alpha and beta MHC isoforms, as well as beta-actin (housekeeping gene); and (ii) separation of MHC isoforms (alpha and beta isoforms) by sodium dodecyl sulfate polyacrylamide gel electrophoresis silver stained.
  • Myocardial gene expressions of alpha and beta mRNA of MHC isoforms were slightly decreased both in nitrofen and CDH fetuses when compared with control fetuses, but evaluation of the alpha-to-beta ratios of MHC isoforms at protein level revealed no significant differences between CDH and control (control, 16.9 +/- 2.5; CDH, 17.0 +/- 2.0).
  • [MeSH-major] Calcium-Transporting ATPases / analysis. Connexin 43 / analysis. Myocardium / metabolism. Myosin Heavy Chains / analysis
  • [MeSH-minor] Animals. Disease Models, Animal. Female. Fetal Organ Maturity / drug effects. Hernia, Diaphragmatic / chemically induced. Hernias, Diaphragmatic, Congenital. Pesticides / pharmacology. Phenyl Ethers / pharmacology. Pregnancy. Protein Isoforms / analysis. Rats. Sarcoplasmic Reticulum Calcium-Transporting ATPases

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  • (PMID = 16952587.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Connexin 43; 0 / Pesticides; 0 / Phenyl Ethers; 0 / Protein Isoforms; 1836-75-5 / nitrofen; EC 3.6.3.8 / Calcium-Transporting ATPases; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; EC 3.6.4.1 / Myosin Heavy Chains
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69. Saidi A, Li T, Weih F, Concannon P, Wang ZQ: Dual functions of Nbs1 in the repair of DNA breaks and proliferation ensure proper V(D)J recombination and T-cell development. Mol Cell Biol; 2010 Dec;30(23):5572-81
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  • Immunodeficiency and lymphoid malignancy are hallmarks of the human disease Nijmegen breakage syndrome (NBS; OMIM 251260), which is caused by NBS1 mutations.
  • Although NBS1 has been shown to bind to the T-cell receptor alpha (TCRα) locus, its role in TCRβ rearrangement is unclear.
  • Here we show that the deletion of the entire Nbs1 protein in T-cell precursors (Nbs1(T-del)) results in severe lymphopenia and a hindrance to the double-negative 3 (DN3)-to-DN4 transition in early T-cell development, due to abnormal TCRβ coding and signal joints as well as the functions of Nbs1 in T-cell expansion.
  • Although a p53 deficiency relieves the DN3→DN4 transition block, neither a p53 deficiency nor ectopic expression of TCRαβ rescues the major T-cell loss in Nbs1(T-del) mice.
  • [MeSH-major] Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. DNA Repair / genetics. DNA Repair / physiology. Genes, Immunoglobulin Heavy Chain. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / metabolism
  • [MeSH-minor] Animals. Base Sequence. Cell Differentiation. Cell Proliferation. DNA Breaks. DNA Primers / genetics. Disease Models, Animal. Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor. Gene Rearrangement, beta-Chain T-Cell Antigen Receptor. Genes, p53. Humans. Lymphopenia / genetics. Lymphopenia / immunology. Lymphopenia / metabolism. Mice. Mice, Knockout. Mutation. Nijmegen Breakage Syndrome / genetics. Nijmegen Breakage Syndrome / immunology. Nijmegen Breakage Syndrome / metabolism. Recombination, Genetic

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  • (PMID = 20921278.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA057569
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / NBN protein, human; 0 / Nijmegen breakage syndrome 1 protein, mouse; 0 / Nuclear Proteins
  • [Other-IDs] NLM/ PMC2976431
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70. Hershberger RE, Norton N, Morales A, Li D, Siegfried JD, Gonzalez-Quintana J: Coding sequence rare variants identified in MYBPC3, MYH6, TPM1, TNNC1, and TNNI3 from 312 patients with familial or idiopathic dilated cardiomyopathy. Circ Cardiovasc Genet; 2010 Apr;3(2):155-61
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  • These variants were 12 MYBPC3 (myosin-binding protein C) in 13 (4.2%) probands, 8 MYH6 (alpha-myosin heavy chain) in 10 (3.2%), 6 TPM1 (tropomyosin) in 6 (1.9%), 4 TNNC1 (cardiac troponin C) in 4 (1.3%), and 1 TNNI3 (cardiac troponin I) in 2 (0.6%).
  • Variants were classified as likely or possibly disease causing in 13 and 20 probands, respectively (n=33; 10.6% overall).
  • One MYH6 variant was classified as unlikely to be disease causing.
  • When combined with our prior resequencing reports, approximately 27% of DCM probands had possible or likely disease-causing variants identified.

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  • (PMID = 20215591.001).
  • [ISSN] 1942-3268
  • [Journal-full-title] Circulation. Cardiovascular genetics
  • [ISO-abbreviation] Circ Cardiovasc Genet
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000334; United States / NHLBI NIH HHS / HV / N01-HV-48194; United States / NHLBI NIH HHS / HL / R01-HL58626; United States / NHLBI NIH HHS / HL / HL058626-10; United States / NCRR NIH HHS / RR / 5 M01 RR000334; United States / NHLBI NIH HHS / HL / R01 HL058626-10; United States / NHLBI NIH HHS / HL / R01 HL058626; United States / NHLBI NIH HHS / HL / N01HV48194
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / MYH6 protein, human; 0 / TPM1 protein, human; 0 / Tropomyosin; 0 / Troponin C; 0 / Troponin I; 0 / myosin-binding protein C; EC 3.6.1.- / Cardiac Myosins; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ NIHMS220802; NLM/ PMC2908892
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71. Mathiyalagan P, Chang L, Du XJ, El-Osta A: Cardiac ventricular chambers are epigenetically distinguishable. Cell Cycle; 2010 Feb 1;9(3):612-7
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  • We have examined gene expression changes and studied histone H3 and H4 acetylation as well as dimethylation of lysine 4 on histone H3 on promoters of alpha-Myosin heavy chain gene (alpha-MHC), beta-Myosin heavy chain gene (beta-MHC), Atrial natriuretic peptide gene (ANp), B-type natriuretic peptide gene (BNP) and Sarcoplasmic reticulum Ca(2+) ATPase gene (SERCA2a).
  • [MeSH-minor] Acetylation. Animals. Chromatin Immunoprecipitation. E1A-Associated p300 Protein / metabolism. Histones / metabolism. Mice. Myosin Heavy Chains / genetics. Myosin Heavy Chains / metabolism. Natriuretic Peptide, Brain / genetics. Natriuretic Peptide, Brain / metabolism. Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism

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  • (PMID = 20090419.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ep300 protein, mouse; 0 / Histones; 114471-18-0 / Natriuretic Peptide, Brain; EC 2.3.1.48 / E1A-Associated p300 Protein; EC 3.6.3.8 / Atp2a2 protein, mouse; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; EC 3.6.4.1 / Myosin Heavy Chains
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72. Zelarayan L, Renger A, Noack C, Zafiriou MP, Gehrke C, van der Nagel R, Dietz R, de Windt L, Bergmann MW: NF-kappaB activation is required for adaptive cardiac hypertrophy. Cardiovasc Res; 2009 Dec 1;84(3):416-24
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  • METHODS AND RESULTS: Cardiac-restricted NF-kappaB inhibition was achieved by expression of a stabilized IkappaBalpha mutant (IkappaBalphaDeltaN) in cells with an active alpha-myosin heavy chain (alphaMHC) promoter employing the Cre/lox technique.
  • [MeSH-minor] Angiotensin II / metabolism. Animals. Apoptosis / physiology. Disease Models, Animal. Female. Fibrosis. I-kappa B Proteins / genetics. I-kappa B Proteins / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Mutation / genetics. Myocardium / metabolism. Myocardium / pathology. Myocytes, Cardiac / metabolism. Myocytes, Cardiac / pathology. Myosin Heavy Chains / metabolism. Receptor, Angiotensin, Type 1 / physiology. Signal Transduction / physiology

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  • (PMID = 19620128.001).
  • [ISSN] 1755-3245
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptor, Angiotensin, Type 1; 11128-99-7 / Angiotensin II; 139874-52-5 / NF-kappaB inhibitor alpha; EC 3.6.4.1 / Myosin Heavy Chains
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73. Feng HZ, Chen M, Weinstein LS, Jin JP: Removal of the N-terminal extension of cardiac troponin I as a functional compensation for impaired myocardial beta-adrenergic signaling. J Biol Chem; 2008 Nov 28;283(48):33384-93
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  • The stimulatory G protein alpha-subunit (Gsalpha) couples the beta-adrenoreceptor to adenylyl cyclase and the intracellular cAMP response.
  • Supporting the hypothesis that up-regulation of cTnI-ND is a compensatory rather than a destructive myocardial response to impaired beta-adrenergic signaling, the aberrant expression of beta-myosin heavy chain in adult Gsalpha-DF but not control mouse hearts was reversed by cTnI overexpression.

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  • (PMID = 18815135.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / AR-048816; United States / NHLBI NIH HHS / HL / HL-078773; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Adrenergic, beta; 0 / Troponin I; EC 3.6.1.- / Ventricular Myosins; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Other-IDs] NLM/ PMC2586242
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74. Nelson TJ, Ge ZD, Van Orman J, Barron M, Rudy-Reil D, Hacker TA, Misra R, Duncan SA, Auchampach JA, Lough JW: Improved cardiac function in infarcted mice after treatment with pluripotent embryonic stem cells. Anat Rec A Discov Mol Cell Evol Biol; 2006 Nov;288(11):1216-24
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  • In the experiments reported here, we transplanted low numbers of two murine ESC lines, respectively engineered to express a beta-galactosidase gene from either a constitutive (elongation factor) or a cardiac-specific (alpha-myosin heavy chain) promoter, into infarcted mouse myocardium.
  • Echocardiographic monitoring of ESC-injected hearts that did not form tumors revealed functional improvements by 4 weeks postinfarction, including significant increases in ejection fraction, circumferential fiber shortening velocity, and peak mitral blood flow velocity.

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  • (PMID = 17004246.001).
  • [ISSN] 1552-4884
  • [Journal-full-title] The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology
  • [ISO-abbreviation] Anat Rec A Discov Mol Cell Evol Biol
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL079277-04; United States / NHLBI NIH HHS / HL / R01 HL079277; United States / NHLBI NIH HHS / HL / HL079277; United States / NHLBI NIH HHS / HL / R01 HL079277-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.1.23 / beta-Galactosidase; EC 3.6.1.- / Cardiac Myosins; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ NIHMS68679; NLM/ PMC2566533
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75. Rastogi S, Mishra S, Gupta RC, Sabbah HN: Reversal of maladaptive gene program in left ventricular myocardium of dogs with heart failure following long-term therapy with the Acorn Cardiac Support Device. Heart Fail Rev; 2005 Jun;10(2):157-63
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  • Therapy with the CSD was associated with up-regulated mRNA expression for alpha-myosin heavy chain and down-regulated mRNA expression of A- and B- type natriuretic peptides, cytokines and favorably modulated cytoskeletal proteins.
  • [MeSH-minor] Animals. Cytokines / genetics. Cytokines / metabolism. Cytoskeletal Proteins / genetics. Cytoskeletal Proteins / metabolism. Disease Models, Animal. Dogs. Myosin Heavy Chains / genetics. Myosin Heavy Chains / metabolism. Natriuretic Peptides / genetics. Natriuretic Peptides / metabolism. RNA, Messenger / metabolism

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  • (PMID = 16258723.001).
  • [ISSN] 1382-4147
  • [Journal-full-title] Heart failure reviews
  • [ISO-abbreviation] Heart Fail Rev
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL074237-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Cytoskeletal Proteins; 0 / Natriuretic Peptides; 0 / RNA, Messenger; EC 3.6.4.1 / Myosin Heavy Chains
  • [Number-of-references] 44
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76. Cheng G, Zhao X, Yan W, Wang W, Zuo X, Huang K, Liu Y, Chen J, Wang J, Cong W, Liu M, Gao H, Chen J, Lu Y, Zheng Z: Alpha interferon is a powerful adjuvant for a recombinant protein vaccine against foot-and-mouth disease virus in swine, and an effective stimulus of in vivo immune response. Vaccine; 2007 Jul 9;25(28):5199-208

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  • [Title] Alpha interferon is a powerful adjuvant for a recombinant protein vaccine against foot-and-mouth disease virus in swine, and an effective stimulus of in vivo immune response.
  • The adjuvant effect of porcine interferon-alpha (PoIFN-alpha) was examined in swine vaccinated with a recombinant FMD protein vaccine named IgG-FMDV, which contains the swine IgG single heavy chain constant region and an immunogenic peptide of serotype O FMDV.
  • The PoIFN-alpha gene was cloned into pcDNA3 vector and the recombinant plasmid was incorporated into cationic liposomes by a dehydration and rehydration procedure to use as an adjuvant, injected together with low-dose IgG-FMDV.
  • As an adjuvant for the protein vaccine, PoIFN-alpha induced strong inflammatory cytokines production in vivo and the results denoted that IFN-adjuvant and our vaccines could drive the immune response toward Th1 type responses.
  • Our studies indicate that porcine IFN-alpha is a powerful adjuvant for recombinant FMD protein vaccine and could aid in vaccination against FMDV in swine.
  • [MeSH-major] Foot-and-Mouth Disease Virus / immunology. Interferon-alpha / immunology. Recombinant Fusion Proteins / immunology. Viral Vaccines / immunology
  • [MeSH-minor] Adjuvants, Immunologic / administration & dosage. Animals. Antibodies, Viral / blood. Cell Line. Cell Proliferation / drug effects. Cytokines / genetics. Cytokines / metabolism. Foot-and-Mouth Disease / blood. Foot-and-Mouth Disease / immunology. Foot-and-Mouth Disease / prevention & control. Gene Expression / drug effects. Immunoglobulin G / genetics. Immunoglobulin G / immunology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Swine. Swine Diseases / immunology. Swine Diseases / prevention & control. Swine Diseases / virology. T-Lymphocytes / cytology. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. Viral Proteins / genetics. Viral Proteins / immunology

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  • (PMID = 17555848.001).
  • [ISSN] 0264-410X
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antibodies, Viral; 0 / Cytokines; 0 / Immunoglobulin G; 0 / Interferon-alpha; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 0 / Viral Proteins; 0 / Viral Vaccines
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77. Li B, Liao YH, Cheng X, Ge H, Guo H, Wang M: Effects of carvedilol on cardiac cytokines expression and remodeling in rat with acute myocardial infarction. Int J Cardiol; 2006 Aug 10;111(2):247-55
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • We studied the effects of 4-weeks therapy with carvedilol starting 24 h after infarction on 1) hemodynamics, 2) tissue weights, 3) myocardial cytokines (TNF-alpha, IL-1beta, IL-6, IL-10 and TGF-beta1) expression by semi-quantitative RT-PCR and immunoblotting, 4) matrix metalloproteinases activity by gelatin zymography, 5) collagen expression by immunohistochemistry, 6) myocardium fetal gene (alpha and beta myosin heavy chain) expression.
  • [MeSH-minor] Animals. Disease Models, Animal. Heart / drug effects. Heart / physiopathology. Interleukin-10 / blood. Interleukin-1beta / blood. Interleukin-6 / blood. Male. Rats. Rats, Wistar. Transforming Growth Factor beta / blood. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 16310260.001).
  • [ISSN] 0167-5273
  • [Journal-full-title] International journal of cardiology
  • [ISO-abbreviation] Int. J. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carbazoles; 0 / Cytokines; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Propanolamines; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 0 / Vasodilator Agents; 0K47UL67F2 / carvedilol; 130068-27-8 / Interleukin-10
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78. Skak K, Haase C, Michelsen BK: Preservation of beta-cell function during immune-mediated, B7-1-dependent alpha-cell destruction. Eur J Immunol; 2005 Sep;35(9):2583-90
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preservation of beta-cell function during immune-mediated, B7-1-dependent alpha-cell destruction.
  • Type 1 diabetes (T1D) is an autoimmune disease in which the pancreatic beta-cells are destroyed in an immune-mediated process.
  • In one mouse model of T1D, the co-expression of the costimulatory molecule, B7-1, and the pro-inflammatory cytokine, tumor necrosis factor (TNF)-alpha, on the beta-cells leads to massive insulitis and loss of beta-cells, resulting in T1D.
  • We show that transgenic mice expressing TNF-alpha on the beta-cells and B7-1 on the alpha-cells are resistant to the development of diabetes despite B7-1-dependent loss of alpha-cells and a massive islet inflammation consisting of T cells, B cells, macrophages and dendritic cells.
  • Furthermore, islets with alpha-cell expression of B7-1 develop alpha-cell destruction and heavy infiltration, but maintain functional beta-cells when they are engrafted into diabetic mice that co-express TNF-alpha and B7-1 on the beta-cells.
  • Thus, our results show that the beta-cells are able to survive in a severely inflamed organ where the neighboring alpha-cells are destroyed, suggesting that in this model B7-1 expression on the target cells is the primary determinant for the loss of islet cells.
  • [MeSH-major] Antigens, CD80 / immunology. Cell Death / immunology. Diabetes Mellitus, Type 1 / immunology. Islets of Langerhans / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Animals. Crosses, Genetic. Glucagon / immunology. Glucagon-Like Peptide 1. Immunohistochemistry. Insulin / immunology. Islets of Langerhans Transplantation. Mice. Mice, Inbred C57BL. Mice, Transgenic. Peptide Fragments / immunology. Protein Precursors / immunology. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric

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  • (PMID = 16078275.001).
  • [ISSN] 0014-2980
  • [Journal-full-title] European journal of immunology
  • [ISO-abbreviation] Eur. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Insulin; 0 / Peptide Fragments; 0 / Protein Precursors; 0 / Tumor Necrosis Factor-alpha; 89750-14-1 / Glucagon-Like Peptide 1; 9007-92-5 / Glucagon
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79. Zhang B, Alaie-Petrillo A, Kon M, Li F, Eckhardt LA: Transcription of a productively rearranged Ig VDJC alpha does not require the presence of HS4 in the IgH 3' regulatory region. J Immunol; 2007 May 15;178(10):6297-306
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcription of a productively rearranged Ig VDJC alpha does not require the presence of HS4 in the IgH 3' regulatory region.
  • If inappropriately applied, however, these processes can mediate genetic changes that lead to disease (e.g., lymphoma).
  • A series of control elements within the Ig H chain (Igh) locus has been implicated in regulating these processes as well as in regulating IgH gene transcription.

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  • (PMID = 17475858.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI030653-17; United States / NIAID NIH HHS / AI / AI030653-17; United States / NIAID NIH HHS / AI / AI30653; United States / NCRR NIH HHS / RR / RR-0307; United States / NIAID NIH HHS / AI / R01 AI030653
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin A; 0 / Immunoglobulin Constant Regions; 0 / Immunoglobulin alpha-Chains
  • [Other-IDs] NLM/ NIHMS125141; NLM/ PMC2724394
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80. Dong J, Thompson AA, Fan Y, Lou J, Conrad F, Ho M, Pires-Alves M, Wilson BA, Stevens RC, Marks JD: A single-domain llama antibody potently inhibits the enzymatic activity of botulinum neurotoxin by binding to the non-catalytic alpha-exosite binding region. J Mol Biol; 2010 Apr 9;397(4):1106-18
The Lens. Cited by Patents in .

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  • [Title] A single-domain llama antibody potently inhibits the enzymatic activity of botulinum neurotoxin by binding to the non-catalytic alpha-exosite binding region.
  • Ingestion or inhalation of botulinum neurotoxin (BoNT) results in botulism, a severe and frequently fatal disease.
  • For treatments that can reverse intoxication, interest has focused on developing inhibitors of the enzymatic BoNT light chain (BoNT Lc).
  • To explore the full range of binding sites for serotype A light chain (BoNT/A Lc) inhibitors, we created a library of non-immune llama single-domain VHH (camelid heavy-chain variable region derived from heavy-chain-only antibody) antibodies displayed on the surface of the yeast Saccharomyces cerevisiae.
  • The structure reveals that the Aa1 VHH binds in the alpha-exosite of the BoNT/A Lc, far from the active site for catalysis.
  • The study validates the utility of non-immune llama VHH libraries as a source of enzyme inhibitors and identifies the BoNT/A Lc alpha-exosite as a target for inhibitor development.

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  • [Copyright] (c) 2010. Published by Elsevier Ltd.
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  • (PMID = 20138889.001).
  • [ISSN] 1089-8638
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] ENG
  • [Databank-accession-numbers] PDB/ 3K3Q
  • [Grant] United States / NIAID NIH HHS / AI / AI057153-06; United States / NIAID NIH HHS / AI / U01 AI075502-03; United States / PHS HHS / / 200-2006-16697; United States / NIAID NIH HHS / AI / AI056493-05; United States / NIAID NIH HHS / AI / AI065359-056070; United States / NIAID NIH HHS / AI / U01 AI056493; United States / NIAID NIH HHS / AI / U54 AI065359-056070; United States / NIAID NIH HHS / AI / U01 AI075502; United States / NIAID NIH HHS / AI / U54 AI065359; United States / NIAID NIH HHS / AI / AI075502-03; United States / NIAID NIH HHS / AI / U01 AI056493-05; United States / NIAID NIH HHS / AI / U54 AI057153; United States / NIAID NIH HHS / AI / U54 AI057153-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antitoxins; 0 / Recombinant Proteins; EC 3.4.24.69 / Botulinum Toxins
  • [Other-IDs] NLM/ NIHMS176079; NLM/ PMC2903050
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81. Rennolds J, Butler S, Maloney K, Boyaka PN, Davis IC, Knoell DL, Parinandi NL, Cormet-Boyaka E: Cadmium regulates the expression of the CFTR chloride channel in human airway epithelial cells. Toxicol Sci; 2010 Jul;116(1):349-58
Hazardous Substances Data Bank. CADMIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cadmium is a toxic heavy metal ranked seventh on the Priority List of Hazardous Substances.
  • It is also a major component of cigarette smoke, and its inhalation is associated with decreased pulmonary function, lung cancer, and chronic obstructive pulmonary disease.
  • We established that the inhibitory effect of cadmium was not a nonspecific effect of heavy metals, as nickel had no effect on CFTR protein levels.
  • Finally, we show that selected antioxidants, including alpha-tocopherol (vitamin E), but not N-acetylcysteine, can prevent the cadmium-induced suppression of CFTR.
  • Future strategies to prevent the deleterious effect of cadmium on epithelial cells and lung functions may benefit from the finding that alpha-tocopherol protects CFTR expression and function.

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  • (PMID = 20363832.001).
  • [ISSN] 1096-0929
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NHLBI NIH HHS / HL / R03HL095442
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 00BH33GNGH / Cadmium; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator
  • [Other-IDs] NLM/ PMC2886859
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82. Lamon S, Wallace MA, Léger B, Russell AP: Regulation of STARS and its downstream targets suggest a novel pathway involved in human skeletal muscle hypertrophy and atrophy. J Physiol; 2009 Apr 15;587(Pt 8):1795-803
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  • Skeletal muscle atrophy is a severe consequence of ageing, neurological disorders and chronic disease.
  • This study aimed to establish if STARS, as well as its downstream signalling targets, RhoA, myocardin-related transcription factors A and B (MRTF-A/B) and serum response factor (SRF), were increased and decreased respectively, in human quadriceps muscle biopsies taken after 8 weeks of both hypertrophy-stimulating resistance training and atrophy-stimulating de-training.
  • The mRNA levels of the SRF target genes involved in muscle structure, function and growth, such as alpha-actin, myosin heavy chain IIa (MHCIIa) and insulin-like growth factor-1 (IGF-1), were also measured.
  • Following resistance training, STARS, MRTF-A, MRTF-B, SRF, alpha-actin, MHCIIa and IGF-1 mRNA, as well as RhoA and nuclear SRF protein levels were all significantly increased by between 1.25- and 3.6-fold.
  • Following the de-training period all measured targets, except for RhoA, which remained elevated, returned to base-line.
  • [MeSH-minor] Adult. Anaerobic Threshold / physiology. Atrophy. Blotting, Western. DNA Primers. DNA-Binding Proteins / physiology. Humans. Hypertrophy. Male. Oncogene Proteins, Fusion / physiology. Oxygen Consumption. Physical Endurance / physiology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Serum Response Factor / physiology. Tomography, X-Ray Computed. Trans-Activators. Weight Lifting / physiology

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  • (PMID = 19255118.001).
  • [ISSN] 1469-7793
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABRA protein, human; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / MKL1 protein, human; 0 / Microfilament Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Serum Response Factor; 0 / Trans-Activators; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2683965
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83. Duda MK, O'Shea KM, Lei B, Barrows BR, Azimzadeh AM, McElfresh TE, Hoit BD, Kop WJ, Stanley WC: Low-carbohydrate/high-fat diet attenuates pressure overload-induced ventricular remodeling and dysfunction. J Card Fail; 2008 May;14(4):327-35
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  • METHODS AND RESULTS: Rats were fed high-carbohydrate diets composed of either starch or sucrose, or a low-carbohydrate/high-fat diet, and underwent abdominal aortic banding (AAB) for 2 months.
  • LV end-diastolic and systolic volumes and the ratio of the mRNA for myosin heavy chain beta/alpha were increased with both high-carbohydrate diets but not with the low-carbohydrate/high-fat diet.

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  • (PMID = 18474346.001).
  • [ISSN] 1532-8414
  • [Journal-full-title] Journal of cardiac failure
  • [ISO-abbreviation] J. Card. Fail.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL074237; United States / NHLBI NIH HHS / HL / P01 HL074237-04; United States / NHLBI NIH HHS / HL / P01 HL074237; United States / NHLBI NIH HHS / HL / P01 HL074237-05; United States / NHLBI NIH HHS / HL / HL074237-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Carbohydrates; 0 / Dietary Fats; 0 / Insulin; 0 / Leptin
  • [Other-IDs] NLM/ NIHMS51935; NLM/ PMC2702243
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84. Romero JM, Aptsiauri N, Vazquez F, Cozar JM, Canton J, Cabrera T, Tallada M, Garrido F, Ruiz-Cabello F: Analysis of the expression of HLA class I, proinflammatory cytokines and chemokines in primary tumors from patients with localized and metastatic renal cell carcinoma. Tissue Antigens; 2006 Oct;68(4):303-10
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • In this study, we compared the tumor expression levels of HLA heavy chain (HLAhc), beta-2-microglobulin (beta2m), chemokines (Interferon-gamma-inducible Protein-10 (IP-10), Interferon-inducible T-cell Alpha-Chemoattractant (I-TAC), Stromal cell-Derived Factor-1 (SDF-1), Macrophage Inflammatory Protein-1-alpha (MIP-1-alpha) and Regulated upon Activation, Normally T-Expressed, and presumably Secreted (RANTES)) and cytokines (Vascular Endothelial Growth Factor (VEGF), Interferon-gamma (IFN-gamma), Interleukin-10 (IL-10), Tumor Growth Factor-beta (TGB-beta)) in primary tumors and adjacent normal tissues from patients with localized and metastatic renal cell carcinoma (RCC) using a quantitative real-time polymerase chain reaction technique.
  • We also observed that disease progression and development of metastasis in RCC are associated with decreased expression of HLAhc, beta2m, IP-10, SDF-1 and IFN-gamma.

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  • (PMID = 17026465.001).
  • [ISSN] 0001-2815
  • [Journal-full-title] Tissue antigens
  • [ISO-abbreviation] Tissue Antigens
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Chemokines; 0 / Cytokines; 0 / Histocompatibility Antigens Class I; 0 / Inflammation Mediators
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85. Zhou Q, Amar S: Identification of proteins differentially expressed in human monocytes exposed to Porphyromonas gingivalis and its purified components by high-throughput immunoblotting. Infect Immun; 2006 Feb;74(2):1204-14
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  • To characterize the roles of Porphyromonas gingivalis and its components in disease processes, we investigated the cytokine profiles induced by live P. gingivalis, its lipopolysaccharide (LPS), and its major fimbrial protein, fimbrillin (FimA).
  • As expected, an extensive repertoire of inflammatory mediators increased subsequent to infection, most predominantly tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), IL-6, IL-10, and granulocyte-macrophage colony-stimulating factor.
  • The expression of proteins involved in gene transcription (e.g., monocyte enhancer factor 2D [MEF2D], signal transducer and activator of transcription 1 [STAT1], STAT3, STAT6, and IL enhancer binding factors [ILF3]), of protein kinases (e.g., mitogen-activated protein kinase 3 [MAPK3], MAP3K8, double-stranded RNA-activated protein kinase [PRKR], and MAP2K4), and of proteins involved in immune responses (e.g., TNF super family member 6 [TNFSF6] and interferon-induced protein with tetratricopeptide repeat 4 [IFIT4]), apoptosis (e.g., genes associated with retinoid interferon-induced mortality 19 [GRIM19]), and other fundamental cellular processes (e.g., clathrin heavy-chain polypeptide, culreticulin, and Ras-associated protein RAB27A) was found to be modulated differentially by P. gingivalis, LPS, and FimA.

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  • (PMID = 16428770.001).
  • [ISSN] 0019-9567
  • [Journal-full-title] Infection and immunity
  • [ISO-abbreviation] Infect. Immun.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R01 DE015989; United States / NIDCR NIH HHS / DE / R01 DE 15989
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Lipopolysaccharides; 0 / fimbrillin; 147680-16-8 / Fimbriae Proteins
  • [Other-IDs] NLM/ PMC1360359
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86. Kawai-Kowase K, Kumar MS, Hoofnagle MH, Yoshida T, Owens GK: PIAS1 activates the expression of smooth muscle cell differentiation marker genes by interacting with serum response factor and class I basic helix-loop-helix proteins. Mol Cell Biol; 2005 Sep;25(18):8009-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although a critical component of vascular disease is modulation of the differentiated state of vascular smooth muscle cells (SMC), the mechanisms governing SMC differentiation are relatively poorly understood.
  • We have previously shown that E-boxes and the ubiquitously expressed class I basic helix-loop-helix (bHLH) proteins, including E2-2 and E12, are important in regulation of the SMC differentiation marker gene, the SM alpha-actin gene.
  • Overexpression of PIAS1 significantly activated the SM alpha-actin promoter and mRNA expression, as well as SM myosin heavy chain and SM22alpha, whereas a small interfering RNA for PIAS1 decreased activity of these promoters, as well as endogenous mRNA expression, and SRF binding to SM alpha-actin promoter within intact chromatin in cultured SMC.
  • Of significance, PIAS1 bound to SRF and activated SM alpha-actin promoter expression in wild-type but not SRF(-/-) e