BioMedLib Search Engine [ goto HOMEPAGE ]

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] An important role of Tyk2 in APC function of dendritic cells for priming CD8+ T cells producing IFN-gamma.

MedlinePlus Health Information. consumer health - Listeria Infections.

COS Scholar Universe. author profiles.

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17048270.001).

[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, Bacterial; 0 / Cytokines; 0 / HLA-A Antigens; 0 / HLA-B Antigens; 0 / OVA-8; 0 / Peptide Fragments; 82115-62-6 / Interferon-gamma; 9006-59-1 / Ovalbumin; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / Tyk2 protein, mouse

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Microtubule-bundling activity of APC is stimulated by interaction with PSD-95.

Adenomatous polyposis coli (APC) tumor suppressor protein binds to microtubules, leading to microtubule bundling and stabilization.

The protein also interacts with postsynaptic density (PSD)-95, a major scaffolding protein in neurons.

Here, we analyzed the effects of PSD-95 on the microtubule-bundling activity of APC.

The coexpression of APC and PSD-95 in COS-7 cells enhanced microtubule-bundle formation compared with the expression of APC alone.

A mutant APC variant that does not associate with PSD-95 did not enhance microtubule bundling, despite coexpression with PSD-95.

Immunoelectron microscopy showed that the APC-PSD-95 complex sometimes colocalized on microtubules in processes of cultured neurons.

These results suggest that the microtubule-bundling activity of APC is regulated by its interaction with PSD-95, which might modulate microtubule architecture and dynamics in neurons.

[MeSH-major] Adenomatous Polyposis Coli Protein / physiology. Microtubules / metabolism. Nerve Tissue Proteins / physiology

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16701944.001).

[ISSN] 0304-3940

[Journal-full-title] Neuroscience letters

[ISO-abbreviation] Neurosci. Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Nerve Tissue Proteins; 0 / postsynaptic density proteins

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Colorectal carcinomas in MUTYH-associated polyposis display histopathological similarities to microsatellite unstable carcinomas.

BACKGROUND: MUTYH-associated polyposis (MAP) is a recessively inherited disorder which predisposes biallelic carriers for a high risk of polyposis and colorectal carcinoma (CRC).

Since about one third of the biallelic MAP patients in population based CRC series has no adenomas, this study aimed to identify specific clinicopathological characteristics of MAP CRCs and compare these with reported data on sporadic and Lynch CRCs.

METHODS: From 44 MAP patients who developed > or = 1 CRCs, 42 of 58 tumours were analyzed histologically and 35 immunohistochemically for p53 and beta-catenin.

KRAS2, the mutation cluster region (MCR) of APC, p53, and SMAD4 were analyzed for somatic mutations.

RESULTS: MAP CRCs frequently localized to the proximal colon (69%, 40/58), were mucinous in 21% (9/42), and had a conspicuous Crohn's like infiltrate reaction in 33% (13/40); all of these parameters occurred at a higher rate than reported for sporadic CRCs.

Tumour infiltrating lymphocytes (TILs) were also highly prevalent in MAP CRCs.

Somatic APC MCR mutations occurred in 14% (5/36) while 64% (23/36) had KRAS2 mutations (22/23 c.34G>T).

CONCLUSION: MAP CRCs show some similarities to micro-satellite unstable cancers, with a preferential proximal location, a high rate of mucinous histotype and increased presence of TILs.

These features should direct the practicing pathologist towards a MAP aetiology of CRC as an alternative for a mismatch repair deficient cause.

High frequent G>T transversions in APC and KRAS2 (mutated in early tumour development) but not in P53 and SMAD4 (implicated in tumour progression) might indicate a predominant MUTYH effect in early carcinogenesis.

[MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. DNA Glycosylases / genetics. Microsatellite Instability

[MeSH-minor] Adult. Aged. Alleles. Cohort Studies. Female. Genetic Predisposition to Disease. Humans. Immunohistochemistry. Lymphocytes, Tumor-Infiltrating / immunology. Male. Middle Aged. Mutation. Tissue Array Analysis

MedlinePlus Health Information. consumer health - Colorectal Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Pathol. 2001 Feb;158(2):527-35 [11159189.001]

[Cites] Cancer Lett. 2008 Sep 18;268(2):308-13 [18495334.001]

[Cites] Br J Cancer. 2001 Sep 1;85(5):692-6 [11531254.001]

[Cites] Nat Genet. 2002 Feb;30(2):227-32 [11818965.001]

[Cites] Am J Pathol. 2003 Feb;162(2):469-77 [12547705.001]

[Cites] N Engl J Med. 2003 Jul 17;349(3):247-57 [12867608.001]

[Cites] Cancer Res. 2003 Nov 15;63(22):7595-9 [14633673.001]

[Cites] Clin Cancer Res. 2004 Feb 1;10(3):972-80 [14871975.001]

[Cites] Lab Invest. 2004 Apr;84(4):493-501 [14968119.001]

[Cites] Br J Cancer. 2004 Apr 19;90(8):1591-3 [15083190.001]

[Cites] Carcinogenesis. 2004 Jul;25(7):1219-26 [14976131.001]

[Cites] Gastroenterology. 2004 Jul;127(1):9-16 [15236166.001]

[Cites] Hum Mol Genet. 2004 Oct 1;13(19):2303-11 [15294875.001]

[Cites] Mod Pathol. 1990 May;3(3):332-5 [2362940.001]

[Cites] Hum Mol Genet. 1992 Jul;1(4):229-33 [1338904.001]

[Cites] Cancer Res. 1994 Jun 1;54(11):3011-20 [8187091.001]

[Cites] Gastroenterology. 1996 Mar;110(3):682-7 [8608876.001]

[Cites] Cancer Res. 1998 Nov 15;58(22):5248-57 [9823339.001]

[Cites] Am J Pathol. 1999 Jun;154(6):1805-13 [10362805.001]

[Cites] Gastroenterology. 1958 Jan;34(1):85-98 [13501357.001]

[Cites] J Natl Cancer Inst. 2004 Nov 3;96(21):1631-4 [15523092.001]

[Cites] Am J Hum Genet. 2005 Jul;77(1):112-9 [15931596.001]

[Cites] Hum Mutat. 2005 Aug;26(2):63-8 [15977173.001]

[Cites] Microsc Res Tech. 2005 May;67(1):15-21 [16025486.001]

[Cites] J Med Genet. 2005 Sep;42(9):e54 [16140997.001]

[Cites] Biochim Biophys Acta. 2005 Nov 25;1756(2):83-96 [16219426.001]

[Cites] Int J Cancer. 2006 Aug 15;119(4):807-14 [16557584.001]

[Cites] Science. 2006 Sep 29;313(5795):1960-4 [17008531.001]

[Cites] J Clin Pathol. 2006 Nov;59(11):1212-5 [16943222.001]

[Cites] Br J Cancer. 2006 Nov 6;95(9):1239-43 [17031395.001]

[Cites] Ann Surg. 2006 Dec;244(6):874-9; discussion 879-80 [17122612.001]

[Cites] Mol Cancer Res. 2007 Feb;5(2):165-70 [17293392.001]

[Cites] Clin Gastroenterol Hepatol. 2007 Mar;5(3):379-87 [17368238.001]

[Cites] Clin Cancer Res. 2008 Jan 1;14(1):139-42 [18172263.001]

[Cites] Clin Cancer Res. 2008 Feb 1;14(3):772-81 [18245538.001]

[Cites] Cancer Biomark. 2008;4(2):55-61 [18503156.001]

[Cites] J Pathol. 2008 Sep;216(1):25-31 [18506705.001]

[Cites] Histopathology. 2008 Aug;53(2):184-94 [18564191.001]

[Cites] Am J Pathol. 2001 Jul;159(1):297-304 [11438476.001]

(PMID = 19527492.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase

[Other-IDs] NLM/ PMC2706846

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The present study characterized more precisely which pathways and cellular events of the allergic response are amplified by DEP in view of the maturation/activation/function of antigen-presenting cells (APC) and the antigen-specific Th response.

We evaluated the effects of DEP on the phenotype and function of bone marrow-derived dendritic cells (BMDC) in vitro and on the expression pattern of APC-related molecules in the murine lung in the presence or absence of antigen in vivo.

In addition, an in vivo experiment showed that repetitive pulmonary exposure to DEP plus antigen (OVA) increased the numbers of MHC class II+cells and those expressing CD11c, DEC205 (DC markers), CD80, CD86 (co-stimulatory molecules), F4/80 (a macrophage marker), and CD19 (a B-cell differentiation antigen) in the lung as compared to that of others (vehicle, DEP, or OVA).

In conclusion, enhancement of allergic responses by DEP can be explained via two novel mechanisms, i.e., enhancement effects on APC including DC and on antigen-specific Th response, which culminate in the promotion of local and systemic dysregulated Th immunity.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19064938.001).

[ISSN] 1535-3702

[Journal-full-title] Experimental biology and medicine (Maywood, N.J.)

[ISO-abbreviation] Exp. Biol. Med. (Maywood)

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens; 0 / Epitopes; 0 / Histocompatibility Antigens Class II; 0 / Immunoglobulins; 0 / Particulate Matter; 0 / Vehicle Emissions; 9006-59-1 / Ovalbumin

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

METHODS: Two multiplex polymerase chain reaction (PCR) assays were developed to detect the 16SrDNA, collagenase (prtC) and fimbria (fimA) genes of P. gingivalis and the 16SrDNA, leukotoxin (lktA) and fimbria-associated protein (fap) genes of A. actinomycetemcomitans in 60 sulcus samples from 30 periodontal healthy subjects and in 122 subgingival plaque samples from 61 patients with CP.

RESULTS: The 16SrDNA, prtC and fimA genes of P. gingivalis were detected in 92.6%, 85.2% and 80.3% of the subgingival plaque samples respectively, while the 16SrDNA, lktA and fap genes of A. actinomycetemcomitans were in 84.4%, 75.4% and 50.0% respectively.

Nucleotide sequence analysis showed 98.62%~100% homology of the PCR products in these genes with the reported sequences. P. gingivalis strains with prtC+/fimA+ and A. actinomycetemcomitans with lktA+ were predominant in deep pockets (>6 mm) or in sites with attachment loss > or =5 mm than in shallow pockets (3~4 mm) or in sites with attachment loss < or =2 mm (P<0.05). P. gingivalis strains with prtC+/fimA+ also showed higher frequency in gingival index (GI)=3 than in GI=1 group (P<0.05).

CONCLUSION: Infection of P. gingivalis with prtC+/fimA+ and A. actinomycetemcomitans with lktA+ correlates with periodontal destruction of CP in Chinese.

Nonetheless P. gingivalis fimA, prtC genes and A. actinomycetemcomitans lktA gene are closely associated with periodontal destruction, while A. actinomycetemcomitans fap gene is not.

[MeSH-minor] Adult. Aged. China / epidemiology. Chronic Disease. Female. Humans. Male. Middle Aged. Prevalence. Risk Assessment / methods. Risk Factors. Species Specificity. Statistics as Topic

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Dent Res. 2001 Oct;80(10):1930-4 [11706954.001]

[Cites] J Periodontal Res. 2004 Apr;39(2):136-42 [15009522.001]

[Cites] J Clin Microbiol. 2004 Sep;42(9):4141-6 [15365002.001]

[Cites] J Bacteriol. 1992 Jun;174(12):3889-95 [1317840.001]

[Cites] J Dent Res. 1993 Jun;72(6):1040-4 [8388414.001]

[Cites] Oral Microbiol Immunol. 1994 Jun;9(3):161-5 [7936722.001]

[Cites] FEMS Microbiol Lett. 1994 Dec 15;124(3):333-41 [7851739.001]

[Cites] Clin Infect Dis. 1995 Jun;20 Suppl 2:S304-7 [7548580.001]

[Cites] J Clin Periodontol. 1996 Mar;23(3 Pt 1):212-9 [8707980.001]

[Cites] Microb Pathog. 1997 Aug;23(2):63-9 [9245617.001]

[Cites] J Clin Microbiol. 1999 May;37(5):1426-30 [10203499.001]

[Cites] Acta Odontol Latinoam. 2004;17(1-2):15-21 [15584257.001]

[Cites] Eur J Oral Sci. 2005 Feb;113(1):28-33 [15693826.001]

[Cites] J Periodontal Res. 2005 Jun;40(3):258-68 [15853973.001]

[Cites] J Periodontol. 2005 May;76(5):674-9 [15898925.001]

[Cites] Eur J Oral Sci. 2005 Jun;113(3):197-202 [15953243.001]

[Cites] J Periodontol. 2005 Feb;76(2):204-9 [15974843.001]

[Cites] Chin Med J (Engl). 2005 Jun 5;118(11):915-21 [15978192.001]

[Cites] J Clin Periodontol. 2005 Aug;32(8):860-6 [15998269.001]

[Cites] Ann Periodontol. 1999 Dec;4(1):1-6 [10863370.001]

[Cites] J Dent Res. 2000 Sep;79(9):1664-8 [11023261.001]

[Cites] Oral Microbiol Immunol. 2000 Feb;15(1):33-9 [11155162.001]

[Cites] J Periodontal Res. 2001 Feb;36(1):18-24 [11246700.001]

[Cites] Periodontol 2000. 2000 Oct;24:153-92 [11276866.001]

[Cites] Crit Rev Oral Biol Med. 2001;12(2):116-24 [11345522.001]

[Cites] Clin Microbiol Infect. 2001 Apr;7(4):213-7 [11422244.001]

[Cites] J Clin Periodontol. 2001 Sep;28(9):886-90 [11493360.001]

[Cites] J Periodontol. 2001 Oct;72(10):1354-63 [11699477.001]

[Cites] J Clin Periodontol. 2001 Dec;28(12):1163-71 [11737515.001]

[Cites] Eur J Oral Sci. 2002 Jun;110(3):212-7 [12120706.001]

[Cites] J Periodontol. 2003 Jan;74(1):90-6 [12593602.001]

[Cites] J Periodontal Res. 2003 Jun;38(3):276-81 [12753365.001]

[Cites] Acta Odontol Scand. 2003 Apr;61(2):115-22 [12790510.001]

[Cites] J Periodontol. 2003 Jul;74(7):1000-6 [12931762.001]

[Cites] Eur J Oral Sci. 2003 Oct;111(5):390-4 [12974681.001]

[Cites] J Clin Microbiol. 2003 Oct;41(10):4829-32 [14532234.001]

[Cites] Curr Protein Pept Sci. 2003 Dec;4(6):443-50 [14683429.001]

[Cites] FEMS Microbiol Lett. 2004 Mar 12;232(1):31-7 [15019731.001]

(PMID = 17266188.001).

[ISSN] 1673-1581

[Journal-full-title] Journal of Zhejiang University. Science. B

[ISO-abbreviation] J Zhejiang Univ Sci B

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Other-IDs] NLM/ PMC1791058

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Identification of candidate cooperative genes of the Apc mutation in transformation of the colon epithelial cell by retroviral insertional mutagenesis.

The mutation of Apc is an important early genetic event in colon carcinogenesis.

To identify cooperative genes for the Apc(Min) mutation the authors carried out retroviral insertional mutagenesis (RIM) using Min mouse-derived IMCE colon epithelial cells.

Anchorage-independent transformed colonies were induced by retroviral infection only in IMCE cells, while no transformation was found in young adult mouse colon (YAMC) cells that are normal for Apc.

These data suggest the importance of cytoskeletal function in Apc-related tumor development and the usefulness of RIM in non-hematopoietic tissues, providing new insight into the early stage of colon carcinogenesis.

[MeSH-major] Cell Transformation, Neoplastic / genetics. Colon / pathology. Genes, APC. Mutagenesis, Insertional. Mutation. Retroviridae / genetics

[MeSH-minor] Animals. Cell Line. Dyneins / genetics. Epithelial Cells / pathology. Membrane Proteins / genetics. Mice. Microtubules / metabolism. Neoplasm Proteins / genetics. Up-Regulation

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18294281.001).

[ISSN] 1349-7006

[Journal-full-title] Cancer science

[ISO-abbreviation] Cancer Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Ahnak protein, mouse; 0 / Membrane Proteins; 0 / Neoplasm Proteins; EC 3.6.4.2 / Dnah3 protein, mouse; EC 3.6.4.2 / Dyneins

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

While several lines of evidence suggest that mutations in adenomatous polyposis coli (APC) may promote chromosome instability, at least in colon cancer, the underlying mechanisms remain unclear.

Here, we turn our attention to GSK-3 - a protein kinase, which in concert with APC, targets beta-catenin for proteolysis - and ask whether GSK-3 is required for accurate chromosome segregation.

Analysis of synchronised HeLa cells shows that GSK-3 inhibitors do not prevent G1/S progression or cell division.

CONCLUSION: Thus, not only do our observations indicate a role for GSK-3 in accurate chromosome segregation, but they also raise the possibility that, if used as therapeutic agents, GSK-3 inhibitors may induce unwanted side effects by inducing chromosome instability.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Cell Sci. 2003 Feb 15;116(Pt 4):637-46 [12538764.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4365-70 [15767571.001]

[Cites] Science. 2005 Mar 25;307(5717):1904-9 [15790842.001]

[Cites] J Cell Sci. 2005 Aug 15;118(Pt 16):3639-52 [16046481.001]

[Cites] Mol Biol Cell. 2005 Oct;16(10):4609-22 [16030254.001]

[Cites] Nat Rev Cancer. 2005 Oct;5(10):773-85 [16195750.001]

[Cites] J Cell Sci. 2005 Oct 15;118(Pt 20):4889-900 [16219694.001]

[Cites] J Cell Biol. 2005 Oct 24;171(2):197-200 [16247021.001]

[Cites] J Cell Sci. 2003 Apr 1;116(Pt 7):1175-86 [12615961.001]

[Cites] J Cell Biol. 2003 Apr 28;161(2):267-80 [12719470.001]

[Cites] EMBO J. 2003 Jun 2;22(11):2752-63 [12773390.001]

[Cites] Science. 2003 Sep 12;301(5639):1547-50 [12970569.001]

[Cites] Mol Cell. 2003 Aug;12(2):381-92 [14536078.001]

[Cites] J Biol Chem. 2003 Nov 14;278(46):45937-45 [12928438.001]

[Cites] Curr Opin Cell Biol. 2003 Dec;15(6):672-83 [14644191.001]

[Cites] J Cell Biol. 2003 Dec 8;163(5):949-61 [14662741.001]

[Cites] J Biol Chem. 2003 Dec 19;278(51):51786-95 [14523000.001]

[Cites] Bioorg Med Chem Lett. 2004 Jan 19;14(2):413-6 [14698171.001]

[Cites] Genes Dev. 2004 Jan 1;18(1):48-61 [14724178.001]

[Cites] Gene. 2005 Nov 21;361:1-12 [16185824.001]

[Cites] Trends Cell Biol. 2005 Nov;15(11):589-98 [16214339.001]

[Cites] Nature. 2006 Apr 13;440(7086):954-8 [16612388.001]

[Cites] EMBO J. 2006 Jun 21;25(12):2814-27 [16763565.001]

[Cites] J Cell Sci. 2006 Sep 1;119(Pt 17):3664-75 [16912073.001]

[Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]

[Cites] J Cell Biol. 2007 Jan 15;176(2):183-95 [17227893.001]

[Cites] Trends Cell Biol. 2005 Sep;15(9):486-93 [16084093.001]

[Cites] Cell. 2003 Feb 21;112(4):407-21 [12600307.001]

[Cites] Diabetes. 2003 Mar;52(3):588-95 [12606497.001]

[Cites] J Cell Biol. 2004 Jan 19;164(2):243-53 [14734535.001]

[Cites] J Cell Sci. 2004 Mar 1;117(Pt 7):1117-28 [14970257.001]

[Cites] J Cell Sci. 2004 Mar 15;117(Pt 8):1577-89 [15020684.001]

[Cites] Trends Biochem Sci. 2004 Feb;29(2):95-102 [15102436.001]

[Cites] Bioorg Med Chem. 2004 Jun 15;12(12):3167-85 [15158785.001]

[Cites] Mol Biol Cell. 2004 Jun;15(6):2978-91 [15075372.001]

[Cites] EMBO J. 2004 Jun 2;23(11):2235-45 [15152189.001]

[Cites] Nat Rev Drug Discov. 2004 Jun;3(6):479-87 [15173837.001]

[Cites] Chromosoma. 2004 Jun;112(8):389-97 [15156327.001]

[Cites] Chromosome Res. 2004;12(6):599-616 [15289666.001]

[Cites] Annu Rev Cell Dev Biol. 2004;20:337-66 [15473844.001]

[Cites] J Cell Sci. 2004 Nov 1;117(Pt 23):5461-77 [15509863.001]

[Cites] Eur J Biochem. 1983 Jan 17;130(1):227-34 [6402364.001]

[Cites] J Cell Sci. 1992 Nov;103 ( Pt 3):665-75 [1478963.001]

[Cites] Mol Cell Biol. 1994 Jan;14(1):831-9 [8264650.001]

[Cites] J Cell Biol. 1994 Dec;127(5):1301-10 [7962091.001]

[Cites] Nature. 1995 Feb 16;373(6515):630-2 [7854422.001]

[Cites] J Cell Biol. 1995 Jun;129(5):1195-204 [7775567.001]

[Cites] Cancer Res. 1995 Jul 15;55(14):2972-7 [7606712.001]

[Cites] J Cell Biol. 1995 Aug;130(4):941-8 [7642709.001]

[Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8455-9 [8710892.001]

[Cites] Curr Biol. 1996 Dec 1;6(12):1664-8 [8994831.001]

[Cites] Science. 1997 Jan 31;275(5300):632-7 [9005842.001]

[Cites] Cell. 1997 May 30;89(5):727-35 [9182760.001]

[Cites] J Cell Sci. 1998 Mar;111 ( Pt 5):557-72 [9454730.001]

[Cites] J Cell Sci. 2004 Dec 15;117(Pt 26):6339-53 [15561772.001]

[Cites] J Cell Biol. 2000 May 15;149(4):761-6 [10811817.001]

[Cites] Nature. 2000 Jul 6;406(6791):86-90 [10894547.001]

[Cites] Chem Biol. 2000 Oct;7(10):793-803 [11033082.001]

[Cites] Mol Med Today. 2000 Dec;6(12):462-9 [11099951.001]

[Cites] Curr Biol. 2001 Jan 9;11(1):44-9 [11166179.001]

[Cites] Nat Cell Biol. 2001 Apr;3(4):429-32 [11283619.001]

[Cites] Nat Cell Biol. 2001 Apr;3(4):433-8 [11283620.001]

[Cites] Diabetes. 2001 May;50(5):937-46 [11334436.001]

[Cites] EMBO Rep. 2001 Jul;2(7):609-14 [11454737.001]

[Cites] Nat Rev Mol Cell Biol. 2001 Oct;2(10):769-76 [11584304.001]

[Cites] J Cell Sci. 2001 Dec;114(Pt 24):4385-95 [11792804.001]

[Cites] J Med Chem. 2002 Mar 14;45(6):1292-9 [11881998.001]

[Cites] Nat Rev Mol Cell Biol. 2002 May;3(5):328-38 [11988767.001]

[Cites] Bioorg Med Chem Lett. 2002 Jun 3;12(11):1525-8 [12031334.001]

[Cites] Diabetes. 2002 Oct;51(10):2903-10 [12351425.001]

[Cites] Nat Rev Mol Cell Biol. 2002 Oct;3(10):731-41 [12360190.001]

[Cites] Curr Biol. 2002 Dec 10;12(23):2055-9 [12477396.001]

(PMID = 17697341.001).

[ISSN] 1471-2121

[Journal-full-title] BMC cell biology

[ISO-abbreviation] BMC Cell Biol.

[Language] ENG

[Grant] United Kingdom / Wellcome Trust / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / beta Catenin; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3

[Other-IDs] NLM/ PMC1976608

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)-driven tumorigenesis.

The majority of sporadic colorectal cancers are triggered by mutations in the adenomatous polyposis coli (APC) tumor suppressor gene, leading to the constitutive activation of the Wnt/beta-catenin signaling pathway and formation of adenomas.

Despite this common genetic basis, colorectal cancers are very heterogeneous in their degree of differentiation, growth rate, and malignancy potential.

Here, we applied a cross-species comparison of expression profiles of intestinal polyps derived from hereditary colorectal cancer patients carrying APC germline mutations and from mice carrying a targeted inactivating mutation in the mouse homologue Apc.

This comparative approach resulted in the establishment of a conserved signature of 166 genes that were differentially expressed between adenomas and normal intestinal mucosa in both species.

Functional analyses of the conserved genes revealed a general increase in cell proliferation and the activation of the Wnt/beta-catenin signaling pathway.

Moreover, the conserved signature was able to resolve expression profiles from hereditary polyposis patients carrying APC germline mutations from those with bi-allelic inactivation of the MYH gene, supporting the usefulness of such comparisons to discriminate among patients with distinct genetic defects.

[MeSH-major] Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli Protein / metabolism. Cell Transformation, Neoplastic / metabolism. Colorectal Neoplasms / pathology. Intestinal Polyps / metabolism

Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

MedlinePlus Health Information. consumer health - Colorectal Cancer.

COS Scholar Universe. author profiles.

GeneTex Inc. NCBI Redirect Page | Genetex Inc. (subscription/membership/fee required).

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

SciCrunch. ArrayExpress: Data: Microarray .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cell. 1995 Jan 27;80(2):285-91 [7834748.001]

[Cites] EMBO J. 1992 Mar;11(3):961-71 [1312467.001]

[Cites] Cancer Res. 2005 Jan 1;65(1):166-76 [15665292.001]

[Cites] Nat Genet. 2002 Feb;30(2):227-32 [11818965.001]

[Cites] Nat Rev Cancer. 2004 Oct;4(10):769-80 [15510158.001]

[Cites] Ai Zheng. 2004 Jul;23(7):737-41 [15248904.001]

[Cites] Cancer Res. 2001 Nov 1;61(21):7722-6 [11691783.001]

[Cites] Oncogene. 1999 May 6;18(18):2883-91 [10362259.001]

[Cites] J Comput Biol. 2000;7(6):819-37 [11382364.001]

[Cites] Nature. 1992 Sep 17;359(6392):235-7 [1528264.001]

[Cites] Cell Signal. 2008 May;20(5):795-802 [18160255.001]

[Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5522-7 [10318916.001]

[Cites] Am J Pathol. 1999 Feb;154(2):515-23 [10027409.001]

[Cites] Genes Dev. 1998 Jan 15;12(2):186-97 [9436979.001]

[Cites] Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):2846-50 [8385345.001]

[Cites] Cell. 1991 Aug 9;66(3):589-600 [1651174.001]

[Cites] Fam Cancer. 2006;5(3):221-6 [16998667.001]

[Cites] Hum Mol Genet. 2003 Oct 15;12 Spec No 2:R159-65 [12915454.001]

[Cites] Cancer Res. 2006 Mar 1;66(5):2514-9 [16510566.001]

[Cites] Trends Mol Med. 2001 Aug;7(8):369-73 [11516998.001]

[Cites] Nat Genet. 2005 Jan;37(1):7-8 [15624012.001]

[Cites] Nature. 1999 Apr 1;398(6726):422-6 [10201372.001]

[Cites] Cell. 2002 Oct 18;111(2):251-63 [12408869.001]

[Cites] Cell. 1991 Aug 9;66(3):601-13 [1678319.001]

[Cites] Cancer Cell. 2003 Sep;4(3):223-38 [14522256.001]

[Cites] Genome Biol. 2007;8(7):R131 [17615082.001]

[Cites] Bioinformatics. 2004 Feb 12;20(3):307-15 [14960456.001]

[Cites] Eur J Biochem. 2003 Oct;270(20):4089-94 [14519120.001]

[Cites] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8969-73 [8090754.001]

[Cites] Crit Rev Oncog. 1995;6(3-6):291-303 [9012588.001]

[Cites] Bioinformatics. 2004 Jan 1;20(1):93-9 [14693814.001]

[Cites] Stat Appl Genet Mol Biol. 2004;3:Article3 [16646809.001]

[Cites] Genome Biol. 2003;4(5):P3 [12734009.001]

[Cites] Science. 1991 Mar 15;251(4999):1366-70 [1848370.001]

[Cites] Cell. 1996 Oct 18;87(2):159-70 [8861899.001]

[Cites] J Biol Chem. 1986 Mar 25;261(9):4239-46 [3081518.001]

[Cites] Science. 1991 Aug 9;253(5020):665-9 [1651563.001]

[Cites] Gastroenterology. 1998 Feb;114(2):275-83 [9453487.001]

[Cites] Gastroenterology. 2007 Feb;132(2):628-32 [17320548.001]

[Cites] Eur J Cancer. 1993;29A(14):1995-2002 [8280495.001]

[Cites] Carcinogenesis. 2005 Jun;26(6):1013-20 [15677630.001]

[Cites] Science. 1995 Jun 2;268(5215):1336-8 [7761852.001]

[Cites] Inflamm Bowel Dis. 2004 Sep;10(5):584-92 [15472519.001]

[Cites] Nat Genet. 2004 Dec;36(12):1306-11 [15565109.001]

[Cites] Eur J Biochem. 1995 Sep 1;232(2):603-10 [7556213.001]

[Cites] Hum Mol Genet. 1992 Jul;1(4):229-33 [1338904.001]

[Cites] Nat Genet. 2005 Jan;37(1):48-55 [15608639.001]

[Cites] Neoplasia. 2001 Jan-Feb;3(1):43-52 [11326315.001]

[Cites] J Pharmacol Exp Ther. 2004 Feb;308(2):434-7 [14610217.001]

[Cites] Mol Cell Biol. 1997 Dec;17(12):7040-6 [9372935.001]

[Cites] News Physiol Sci. 2003 Apr;18:60-4 [12644621.001]

[Cites] J Cell Biochem. 1997 Mar 1;64(3):514-23 [9057109.001]

[Cites] BMC Bioinformatics. 2005;6:192 [16048644.001]

[Cites] Bioinformatics. 2002;18 Suppl 1:S96-104 [12169536.001]

[Cites] Nucleic Acids Res. 2004;32(19):e146 [15514107.001]

[Cites] J Biochem Mol Biol. 2005 Jan 31;38(1):9-16 [15715940.001]

[Cites] Biochim Biophys Acta. 2007 Jan;1775(1):103-37 [17010523.001]

[Cites] Cell. 2006 Jun 30;125(7):1230-3 [16814709.001]

[Cites] Nat Rev Cancer. 2001 Oct;1(1):55-67 [11900252.001]

(PMID = 18403596.001).

[ISSN] 1525-2191

[Journal-full-title] The American journal of pathology

[ISO-abbreviation] Am. J. Pathol.

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G0301154

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein

[Other-IDs] NLM/ PMC2329845

   

Advertisement

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular insights into mammalian end-binding protein heterodimerization.

Microtubule plus-end tracking proteins (+TIPs) are involved in many microtubule-based processes.

End binding (EB) proteins constitute a highly conserved family of +TIPs.

Here we used a combination of methods to investigate the dimerization properties of the three human EB proteins EB1, EB2, and EB3.

Based on Förster resonance energy transfer, we demonstrate that the C-terminal dimerization domains of EBs (EBc) can readily exchange their chains in solution.

We further document that EB1c and EB3c preferentially form heterodimers, whereas EB2c does not participate significantly in the formation of heterotypic complexes.

Fluorescence spectroscopy and nuclear magnetic resonance studies in the presence of the cytoskeleton-associated protein-glycine-rich domains of either CLIP-170 or p150(glued) or of a fragment derived from the adenomatous polyposis coli tumor suppressor protein show that chain exchange of EBc domains can be controlled by binding partners.

Extension of these studies of the EBc domains to full-length EBs demonstrate that heterodimer formation between EB1 and EB3, but not between EB2 and the other two EBs, occurs both in vitro and in cells as revealed by live cell imaging.

[MeSH-major] Microtubule-Associated Proteins / metabolism. Models, Molecular. Protein Multimerization / physiology

[MeSH-minor] Animals. CHO Cells. Cell Line. Cricetinae. Cricetulus. Humans. Kinetics. Magnetic Resonance Spectroscopy. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Protein Structure, Quaternary. Protein Structure, Tertiary. Recombinant Proteins / chemistry. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Spectrometry, Fluorescence

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Mol Biol Cell. 2002 Oct;13(10):3627-45 [12388762.001]

[Cites] Acta Crystallogr D Biol Crystallogr. 2002 Nov;58(Pt 11):1948-54 [12393927.001]

[Cites] J Biol Chem. 2003 Sep 19;278(38):36430-4 [12857735.001]

[Cites] J Biol Chem. 2003 Oct 3;278(40):38926-34 [12860982.001]

[Cites] J Biol Chem. 2003 Dec 12;278(50):49721-31 [14514668.001]

[Cites] Neuron. 2004 Jun 24;42(6):897-912 [15207235.001]

[Cites] Nat Cell Biol. 2004 Sep;6(9):820-30 [15311282.001]

[Cites] Adv Protein Chem. 1966;21:287-386 [5333290.001]

[Cites] Annu Rev Biochem. 1972;41:903-24 [4563445.001]

[Cites] J Mol Biol. 1979 Oct 15;134(1):75-94 [537062.001]

[Cites] Biochemistry. 1988 Oct 18;27(21):8063-8 [3233195.001]

[Cites] Proteins. 1993 Sep;17(1):75-86 [8234246.001]

[Cites] J Mol Biol. 1993 Dec 5;234(3):779-815 [8254673.001]

[Cites] Adv Protein Chem. 1995;46:141-76 [7771317.001]

[Cites] J Mol Graph. 1996 Feb;14(1):51-5, 29-32 [8744573.001]

[Cites] Annu Rev Cell Dev Biol. 1997;13:83-117 [9442869.001]

[Cites] Biochemistry. 1999 Jan 19;38(3):870-80 [9893981.001]

[Cites] EMBO J. 2005 Jan 26;24(2):261-9 [15616574.001]

[Cites] J Cell Biol. 2005 Feb 14;168(4):587-98 [15699215.001]

[Cites] J Cell Biol. 2005 Sep 12;170(6):895-901 [16157700.001]

[Cites] Mol Cell. 2006 Sep 1;23(5):663-71 [16949363.001]

[Cites] Cell. 2006 Dec 29;127(7):1415-24 [17190604.001]

[Cites] PLoS Biol. 2007 Feb;5(2):e29 [17227146.001]

[Cites] Curr Biol. 2007 Jul 3;17(13):1134-9 [17600711.001]

[Cites] Curr Biol. 2007 Aug 7;17(15):1318-25 [17658256.001]

[Cites] Trends Biochem Sci. 2007 Sep;32(9):407-14 [17764955.001]

[Cites] Mol Cell. 2007 Sep 21;27(6):976-91 [17889670.001]

[Cites] Nat Struct Mol Biol. 2007 Oct;14(10):959-67 [17828277.001]

[Cites] Exp Cell Res. 2008 Jan 1;314(1):213-26 [17964570.001]

[Cites] Nature. 2007 Dec 13;450(7172):1100-5 [18059460.001]

[Cites] Nat Rev Mol Cell Biol. 2008 Apr;9(4):309-22 [18322465.001]

[Cites] Nat Cell Biol. 2008 Apr;10(4):415-21 [18364701.001]

[Cites] Oncogene. 2008 Apr 10;27(17):2494-500 [17968321.001]

[Cites] Nat Cell Biol. 2008 Oct;10(10):1181-9 [18806788.001]

[Cites] Trends Biochem Sci. 2008 Nov;33(11):535-45 [18835717.001]

[Cites] J Cell Biol. 2008 Dec 29;183(7):1223-33 [19103809.001]

[Cites] Neuron. 2009 Jan 15;61(1):85-100 [19146815.001]

[Cites] J Cell Biol. 2009 Mar 9;184(5):691-706 [19255245.001]

[Cites] Mol Biol Cell. 2009 Jun;20(11):2684-96 [19369422.001]

[Cites] Cell. 2009 Jul 23;138(2):366-76 [19632184.001]

[Cites] J Biol Chem. 2009 Oct 9;284(41):28367-81 [19696028.001]

[Cites] Oncogene. 2000 Jan 13;19(2):210-6 [10644998.001]

[Cites] J Cell Biol. 2000 May 15;149(4):761-6 [10811817.001]

[Cites] Genomics. 2001 Jan 15;71(2):142-9 [11161807.001]

[Cites] Cell. 2001 May 18;105(4):421-4 [11371339.001]

[Cites] Biotechniques. 2001 Jul;31(1):88-90, 92 [11464525.001]

[Cites] Nature. 2003 Apr 17;422(6933):753-8 [12700769.001]

(PMID = 20008324.001).

[ISSN] 1083-351X

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / MAPRE1 protein, human; 0 / MAPRE3 protein, human; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; 144198-36-7 / dynactin; 148349-95-5 / cytoplasmic linker protein 170

[Other-IDs] NLM/ PMC2820806

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

A causal link for COX-2 in epithelial tumorigenesis was shown in genetically manipulated animal models of colon and breast carcinoma.

COX enzymes are targets for cancer prevention as shown by the observation that nonselective COX and selective COX-2 inhibitors have been reported to effectively prevent experimental colon cancer and can regress colorectal polyps in patients with familial adenomatous polyposis.

Genetic Alliance. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16688727.001).

[ISSN] 0899-1987

[Journal-full-title] Molecular carcinogenesis

[ISO-abbreviation] Mol. Carcinog.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Prostaglandins; EC 1.14.99.1 / Cyclooxygenase 2

[Number-of-references] 53

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Fibroblast growth factor 9 has oncogenic activity and is a downstream target of Wnt signaling in ovarian endometrioid adenocarcinomas.

Roughly 40% of ovarian endometrioid adenocarcinomas (OEA) have constitutive activation of Wnt signaling as a result of oncogenic mutations in the beta-catenin protein or inactivating mutations in key negative regulators of beta-catenin, such as the adenomatous polyposis coli and Axin tumor suppressor proteins.

Using microarray and quantitative PCR-based approaches, we found that fibroblast growth factor (FGF9) expression was increased >6-fold in primary OEAs with Wnt/beta-catenin pathway defects compared with OEAs lacking such defects.

[MeSH-major] Carcinoma, Endometrioid / genetics. Fibroblast Growth Factor 9 / genetics. Ovarian Neoplasms / genetics. Wnt1 Protein / metabolism

MedlinePlus Health Information. consumer health - Ovarian Cancer.

COS Scholar Universe. author profiles.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16452189.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / PHS HHS / / NIH P30 46952; United States / NCI NIH HHS / CA / R01 CA 85463; United States / NCI NIH HHS / CA / R01 CA 94172; United States / NCI NIH HHS / CA / U19 CA 84953

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / FGF9 protein, human; 0 / Fibroblast Growth Factor 9; 0 / RNA, Messenger; 0 / Wnt1 Protein; 0 / beta Catenin

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Not-so-pseudo a substrate: Acm1-mediated inhibition of the APC.

In a recent issue of Molecular Cell, Enquist-Newman et al. (2008) demonstrate that Acm1 is ubiquitinated by APC(Cdc20).

By contrast, the high-affinity interaction between Acm1 and APC(Cdh1) renders it a poor substrate, but a specific inhibitor, of the APC(Cdh1) complex.

[MeSH-major] Repressor Proteins / metabolism. Saccharomyces cerevisiae / metabolism. Saccharomyces cerevisiae Proteins / metabolism. Ubiquitin-Protein Ligase Complexes / antagonists & inhibitors. Ubiquitin-Protein Ligase Complexes / metabolism

[MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Cdc20 Proteins. Cdh1 Proteins. Cell Cycle Proteins / metabolism. Mitosis. Substrate Specificity. Ubiquitination

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

Saccharomyces Genome Database. Saccharomyces Genome Database .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentOn] Mol Cell. 2008 May 23;30(4):437-46 [18498748.001]

(PMID = 18538651.001).

[ISSN] 1097-4164

[Journal-full-title] Molecular cell

[ISO-abbreviation] Mol. Cell

[Language] eng

[Publication-type] Comment; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Acm1 protein, S cerevisiae; 0 / CDC20 protein, S cerevisiae; 0 / CDH1 protein, S cerevisiae; 0 / Cdc20 Proteins; 0 / Cdh1 Proteins; 0 / Cell Cycle Proteins; 0 / Repressor Proteins; 0 / Saccharomyces cerevisiae Proteins; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

High level of nutrients and water activity, direct contact with soil, and lack of thermal procedures during primary processing make fresh produce a potential food safety hazard.

Aerobic plate counts (APC) of dilutions were determined.

Statistical analysis (least significant difference-based analysis of variance) showed that there were no significant (P > 0.05) differences in APC among control, water at 25 degrees C, and 5% acetic acid at 25 degrees C.

Thermal treatments with water at 95 degrees C, and 5% acetic acid at 95 degrees C, were both significantly (P < 0.05) more effective in APC reduction than were nonthermal treatments, but were not significantly different from each other.

Results indicated that a thermal water immersion intervention in primary processing of fresh melons can result in a 3-log reduction of natural microflora surface contamination, but 5% acetic acid will not significantly augment this reduction.

MedlinePlus Health Information. consumer health - Foodborne Illness.

Hazardous Substances Data Bank. ACETIC ACID .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20501053.001).

[ISSN] 0362-028X

[Journal-full-title] Journal of food protection

[ISO-abbreviation] J. Food Prot.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Infective Agents, Local; Q40Q9N063P / Acetic Acid

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

This recognition results in the formation of a so-called immune synapse (IS) at the T-cell/APC interface, which is crucial for T-cell activation.

Dynamic analysis of T-cell/APC interaction by AFM revealed that in the presence of antigen interaction forces increased from 1 to 2 nN at early time-points to a maximum of approximately 14 nN after 30 min and decreased again after 60 min.

BIRT377 almost completely abolish the interaction forces, emphasizing the importance of LFA-1/ICAM-1-interactions for firm T-cell/APC adhesion.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Immunol. 1999 Nov 15;163(10):5173-7 [10553036.001]

[Cites] Nat Cell Biol. 2000 Jun;2(6):313-7 [10854320.001]

[Cites] Curr Biol. 2000 Dec 14-28;10(24):R923-33 [11137031.001]

[Cites] Biophys J. 2002 Oct;83(4):2270-9 [12324444.001]

[Cites] Cells Tissues Organs. 2002;172(3):174-89 [12476047.001]

[Cites] J Leukoc Biol. 2003 Jan;73(1):30-48 [12525560.001]

[Cites] Eur J Immunol. 2003 Feb;33(2):411-21 [12645938.001]

[Cites] Nat Rev Immunol. 2003 Nov;3(11):867-78 [14668803.001]

[Cites] Blood. 2004 Nov 1;104(9):2801-9 [15256430.001]

[Cites] J Biol Chem. 1992 Dec 25;267(36):25864-72 [1464601.001]

[Cites] Blood. 1993 Jan 15;81(2):419-23 [8422461.001]

[Cites] J Exp Med. 1993 Oct 1;178(4):1453-8 [7690835.001]

[Cites] Science. 1994 Oct 14;266(5183):257-9 [7939660.001]

[Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3477-81 [8622961.001]

[Cites] Nature. 1998 Sep 3;395(6697):82-6 [9738502.001]

[Cites] Science. 1999 Jul 9;285(5425):221-7 [10398592.001]

[Cites] J Biol Chem. 2005 Feb 11;280(6):4753-60 [15550395.001]

[Cites] PLoS Biol. 2005 Jun;3(6):e150 [15857154.001]

[Cites] Nat Rev Immunol. 2005 Jul;5(7):546-59 [15965491.001]

[Cites] Eur J Immunol. 2005 Jun;35(6):1741-53 [15909310.001]

[Cites] Semin Immunol. 2005 Dec;17(6):442-51 [16263308.001]

[Cites] Exp Biol Med (Maywood). 2006 Sep;231(8):1306-12 [16946399.001]

[Cites] Biophys J. 2008 Aug;95(3):1448-59 [18456832.001]

[Cites] Nat Nanotechnol. 2008 May;3(5):261-9 [18654521.001]

[Cites] Nature. 2008 Oct 9;455(7214):764-9 [18843362.001]

[Cites] Curr Opin Cell Biol. 2006 Oct;18(5):579-86 [16904883.001]

[Cites] Biomacromolecules. 2006 Nov;7(11):3188-95 [17096550.001]

[Cites] Immunity. 2007 Jan;26(1):17-27 [17241958.001]

[Cites] Science. 2007 Jan 26;315(5811):528-31 [17185562.001]

[Cites] J Immunol. 2007 Mar 15;178(6):3637-47 [17339461.001]

[Cites] Blood. 2007 Sep 1;110(5):1519-29 [17392507.001]

[Cites] J Cell Sci. 2008 Jun 1;121(11):1785-91 [18492792.001]

[Cites] J Immunol Methods. 2008 Jul 31;336(2):91-7 [18539294.001]

[ErratumIn] Proc Natl Acad Sci U S A. 2010 Feb 2;107(5):2373

(PMID = 19822763.001).

[ISSN] 1091-6490

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] ENG

[Grant] United States / NEI NIH HHS / EY / PN2 EY016586

[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 / BIRT 377; 0 / Imidazolidines; 0 / Lymphocyte Function-Associated Antigen-1; 0 / Peptide Fragments; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 3.2.1.- / hen egg lysozyme; EC 3.2.1.17 / Muramidase

[Other-IDs] NLM/ PMC2764924

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We investigated whether the circadian clock modulated core molecular processes necessary for memory formation in vivo by analyzing circadian regulation of basal and LTS-induced levels of phosphorylated mitogen-activated protein kinase (P-MAPK) and Aplysia CCAAT/enhancer binding protein (ApC/EBP).

In contrast, the circadian clock regulated basal levels of ApC/EBP protein with peak levels at night, antiphase to the rhythm in LTS.

Importantly, LTS training during the (subjective) day produced greater increases in P-MAPK and ApC/EBP than training at night.

Thus, circadian modulation of LTS occurs, at least in part, by suppressing changes in key proteins at night.

Rescue of long-term memory formation at night required both facilitation of MAPK and transcription in conjunction with LTS training, confirming that the circadian clock at night actively suppresses MAPK activation and transcription involved in memory formation.

The circadian clock appears to modulate LTS at multiple levels.

Together, our studies suggest that the circadian clock modulates LTS at multiple steps and locations during the formation of long-term memory.

[MeSH-minor] Animals. CCAAT-Enhancer-Binding Proteins / metabolism. Electric Stimulation / methods. Enzyme Activation / physiology. Ganglia, Invertebrate / enzymology. Hemolymph / metabolism. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Serotonin / metabolism

MedlinePlus Health Information. consumer health - Memory.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16928854.001).

[ISSN] 1529-2401

[Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience

[ISO-abbreviation] J. Neurosci.

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / NS050589

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 333DO1RDJY / Serotonin; EC 2.7.11.24 / Mitogen-Activated Protein Kinases

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cardiovascular protective role for activated protein C during endotoxemia in rats.

OBJECTIVE: We examined whether activated protein C (APC) treatment improves cardiovascular inflammation and dysfunction in endotoxemic rats.

INTERVENTIONS: Internal carotid artery and external jugular vein were catheterized under sterile conditions in rats.

Instrumented rats infused or not with APC (240 microg/kg per hour) were challenged with E. coli endotoxin (10 mg/kg).

MEASUREMENTS AND RESULTS: Endotoxin administration induced systemic hypotension, depression of myocardial systolic performance and reduction in capillary density of the small intestine muscularis layer.

Plasma levels of nitrite/nitrate, tumor necrosis factor alpha and macrophage migration inhibitory factor, mesentery venule leukocyte-endothelium interactions, heart and small intestine myeloperoxidase activities were increased in endotoxin-treated rats.

APC largely prevented endotoxin-induced cardiovascular dysfunction with improved systemic hemodynamics, functional capillary density, and myocardial contractile performance.

Beneficial cardiovascular effects of APC were associated with attenuation of entotoxin-induced inflammatory response in terms of plasma levels of nitrite/nitrate, tumor necrosis factor alpha, macrophage migration inhibitory factor, and endothelial cell-leukocyte activation.

CONCLUSION: APC reduces systemic and tissue inflammation and preserves cardiovascular function during experimental endotoxemia.

[MeSH-major] Cardiovascular System / drug effects. Endotoxemia. Protein C Inhibitor / pharmacology. Serine Proteinase Inhibitors / pharmacology

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Br J Anaesth. 2004 Jul;93(1):114-20 [15121730.001]

[Cites] Circ Res. 2005 May 27;96(10):1095-102 [15879312.001]

[Cites] J Biol Chem. 2001 Apr 6;276(14):11199-203 [11278252.001]

[Cites] Neuron. 2004 Feb 19;41(4):563-72 [14980205.001]

[Cites] Crit Care Med. 2004 Apr;32(4):1011-7 [15071394.001]

[Cites] Circulation. 2001 Sep 4;104(10):1171-5 [11535575.001]

[Cites] Lancet. 2005 Jan 1-7;365(9453):63-78 [15639681.001]

[Cites] Curr Opin Infect Dis. 2004 Jun;17(3):205-11 [15166822.001]

[Cites] N Engl J Med. 1989 Aug 3;321(5):280-7 [2664516.001]

[Cites] Trends Immunol. 2004 Oct;25(10):536-42 [15364056.001]

[Cites] Blood. 2000 Jun 15;95(12):3781-7 [10845910.001]

[Cites] Nat Med. 2004 Dec;10(12):1379-83 [15516929.001]

[Cites] Shock. 2004 Mar;21(3):222-9 [14770034.001]

[Cites] Intensive Care Med. 2005 Nov;31(11):1573-6 [16175347.001]

[Cites] Nat Med. 2003 Mar;9(3):338-42 [12563316.001]

[Cites] Crit Care Med. 2003 Mar;31(3):834-40 [12626993.001]

[Cites] N Engl J Med. 2001 Mar 8;344(10 ):699-709 [11236773.001]

[Cites] Biochem Soc Trans. 2005 Apr;33(Pt 2):401-5 [15787615.001]

[Cites] N Engl J Med. 2003 Jan 9;348(2):138-50 [12519925.001]

[Cites] Crit Care Med. 2005 Feb;33(2):368-72 [15699841.001]

[Cites] J Am Coll Cardiol. 2004 Jun 16;43(12):2348-58 [15193704.001]

(PMID = 16601957.001).

[ISSN] 0342-4642

[Journal-full-title] Intensive care medicine

[ISO-abbreviation] Intensive Care Med

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Protein C Inhibitor; 0 / Serine Proteinase Inhibitors

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

To address this missing information, a total of 2,548 sponge samples from pelts, preevisceration carcasses, and postintervention carcasses were collected from multiple large commercial lamb processing plants to determine aerobic plate counts, the prevalences of Escherichia coli O157:H7, non-O157 Shiga toxin-producing E. coli (STEC), and Salmonella.

The prevalences of E. coli O157:H7 from the pelts, the preevisceration carcasses, and the postintervention carcasses were 12.8, 1.6, and 2.9%, respectively.

The average Salmonella prevalences were 14.4, 4.3, and 1.8% for pelts, preevisceration carcasses, and postintervention carcasses, respectively.

A small number of STEC serotypes associated with severe human illness were isolated from postintervention carcasses.

The results of this study establish a baseline for microbiological quality and prevalences of Salmonella, E. coli O157:H7, and STEC in U.S. lamb processing plants.

[MeSH-major] Escherichia coli / isolation & purification. Food Contamination / analysis. Food-Processing Industry / standards. Salmonella / isolation & purification. Sheep / microbiology

[MeSH-minor] Abattoirs. Animals. Colony Count, Microbial. Consumer Product Safety. Escherichia coli O157 / isolation & purification. Food Microbiology. Humans. Meat / microbiology. Prevalence. Serotyping. United States

MedlinePlus Health Information. consumer health - Foodborne Illness.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17803136.001).

[ISSN] 0362-028X

[Journal-full-title] Journal of food protection

[ISO-abbreviation] J. Food Prot.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] APC, MYH, and the correlation genotype-phenotype in colorectal polyposis.

BACKGROUND: Familial adenomatous polyposis (FAP) has been divided into two entities: classical (CFAP) and attenuated (AFAP).

With the discovery of MYH associated polyposis (MAP) syndrome, the clinical differences have become unclear.

The aim of our study was to investigate patients with polyposis treated in our institution for a correlation between genotype and phenotype.

Four groups were identified: AFAP, CFAP, MAP, and no-mutation patients.

RESULTS: Patient breakdown was CFAP patients (n = 322/294), AFAP patients (n = 13/41), MYH patients (n = 17) and no-mut patients (n = 32).

Patients not tested for APC mutation (n = 131) were excluded.

Major differences were found for MYH patients: later age at diagnosis, more cancers, fewer polyps, and more located in the right part of the colon.

For phenotype/genotype correlation, patients aged more than 35 years at the time of colectomy and with fewer than 100 polyps had significantly more mutation found on MYH.

CONCLUSIONS: This two-way analysis did not show any correlation that might help to identify a subgroup of patients with APC mutation that may be considered attenuated.

It is more likely that the MAP syndrome is the real AFAP.

[MeSH-major] Adenomatous Polyposis Coli / genetics. DNA Glycosylases / genetics. Genes, APC

[MeSH-minor] Adolescent. Adult. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Mutation. Phenotype. Syndrome. Young Adult

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19169759.001).

[ISSN] 1534-4681

[Journal-full-title] Annals of surgical oncology

[ISO-abbreviation] Ann. Surg. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Novel human pathological mutations. Gene symbol: APC. Disease: adenomatous polyposis coli.

[MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. INDEL Mutation

Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19320041.001).

[ISSN] 1432-1203

[Journal-full-title] Human genetics

[ISO-abbreviation] Hum. Genet.

[Language] eng

[Databank-accession-numbers] GENBANK/ HX080001

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Codon; 0 / Codon, Nonsense

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Graft-versus-Host Disease (GvHD) is the most serious complication of allogeneic stem cell transplantation (SCT) and results from an activation of donor lymphocytes by recipient antigen-presenting cells (APCs).

For a long time, it has been postulated that the intestinal microflora and endotoxin exert a crucial step in this APC activation, as there is early and severe gastrointestinal damage induced by pretransplant conditioning.

With the detailed description of pathogen-associated molecular patterns and pathogen recognition receptors single nucleotide polymorphisms of TLRs and especially NOD2 have been identified as potential risk factors of GvHD and transplant related complications thus further supporting the crucial role of innate immunity in SCT, related complications.

Gastrointestinal decontamination and neutralization of endotoxin have been used to interfere with this early axis of activation with some success but more specific approaches of modulation of innate immunity are needed for further improvement of clinical outcome.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21188220.001).

[ISSN] 2042-0099

[Journal-full-title] International journal of inflammation

[ISO-abbreviation] Int J Inflam

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC3003997

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

This is achieved by the action of ubiquitin ligases (E3s), which remove both negative and positive regulators of the cell cycle.

Though our current understanding of the plant cell cycle has improved a lot these recent years, the identity of the E3s regulating it and their mode of action is still in its infancy.

Thus the anaphase promoting complex/cyclosome (APC/C) not only controls mitotic events, but is also important in post-mitotic cells for normal plant development and cell differentiation.

[MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Models, Biological. Plant Growth Regulators / metabolism. Ubiquitin-Protein Ligase Complexes / genetics. Ubiquitin-Protein Ligase Complexes / metabolism. Ubiquitin-Protein Ligases / genetics. Ubiquitin-Protein Ligases / metabolism

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.

(PMID = 20810305.001).

[ISSN] 1879-0356

[Journal-full-title] Current opinion in plant biology

[ISO-abbreviation] Curr. Opin. Plant Biol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Plant Growth Regulators; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

In turn, Tome-1 itself is targeted for degradation by APC in the G1 phase of the cell cycle.

[MeSH-major] Cell Cycle / genetics. Cell Cycle Proteins / genetics. Promoter Regions, Genetic / genetics

[MeSH-minor] 5' Flanking Region / genetics. Animals. Base Sequence. Cell Division. Down-Regulation / genetics. G2 Phase. Humans. Mice. Molecular Sequence Data. Mutation / genetics. NIH 3T3 Cells. Sequence Alignment. Transcriptional Activation / genetics

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15733861.001).

[ISSN] 0014-5793

[Journal-full-title] FEBS letters

[ISO-abbreviation] FEBS Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / CDCA3 protein, human; 0 / Cell Cycle Proteins; 0 / Tome-1 protein, mouse

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

OBJECTIVE: Debate exists as to the benefits of performing mucosectomy as part of pouch surgery for ulcerative colitis (UC) and familial adenomatous polyposis (FAP).

Potential reasons for functional problems were investigated, as were rates of 'cuffitis', dysplasia, polyposis and cancer in the ileal pouch and anal canal.

Meta-analysis suggested that nighttime seepage of stool and resting and squeeze pressure were worse after mucosectomy.

Mucosectomy does seem to confer benefit in terms of disease control but this benefit does not reach statistical significance.

Performing mucosectomy results in some clinical benefits in terms of lower rates of inflammation and dysplasia in the retained mucosa in UC patients and lower rates of cuff polyposis in FAP patients.

However, on the basis of available evidence mucosectomy is only indicated in those cases where the patient is at a high risk of disease in the retained rectal cuff.

[MeSH-major] Colonic Pouches / adverse effects. Intestinal Mucosa / surgery. Proctocolectomy, Restorative / adverse effects

[MeSH-minor] Adenocarcinoma / prevention & control. Adenomatous Polyposis Coli / surgery. Anastomosis, Surgical / adverse effects. Anastomosis, Surgical / methods. Anus Neoplasms / prevention & control. Arsenates. Colitis, Ulcerative / surgery. Humans. Ileal Neoplasms / prevention & control. Randomized Controlled Trials as Topic

Hazardous Substances Data Bank. ARSENIC ACID .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17504334.001).

[ISSN] 1462-8910

[Journal-full-title] Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland

[ISO-abbreviation] Colorectal Dis

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Arsenates; N7CIZ75ZPN / arsenic acid

[Number-of-references] 70

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Active systemic lupus erythematosus is associated with failure of antigen-presenting cells to express programmed death ligand-1.

OBJECTIVE: Antigen-presenting cells (APC) play critical roles in establishing and maintaining peripheral tolerance.

This is accomplished in part via expression of negative co-stimulatory molecules such as programmed death ligand-1 (PD-L1) on tolerogenic APC, such as immature myeloid dendritic cells (mDC).

Several studies have strongly linked dysfunction of APC, including mDC, to the pathogenesis of SLE.

The objective of this study was to determine whether APC expressed PD-L1 protein at normal levels during active lupus.

In contrast, both mDC and Mo from patients with active SLE failed to up-regulate PD-L1 over a 5 day time course, expressing this protein only during disease remissions.

CONCLUSIONS: These data are the first to link active lupus with reversibly decreased PD-L1 expression on professional APC, suggesting a novel mechanism for loss of peripheral tolerance in SLE.

Genetic Alliance. consumer health - Lupus.

Genetic Alliance. consumer health - Systemic lupus erythematosus.

MedlinePlus Health Information. consumer health - Lupus.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Transplantation. 2007 Mar 27;83(6):774-82 [17414712.001]

[Cites] Nat Med. 1999 Dec;5(12):1365-9 [10581077.001]

[Cites] Lupus. 2000;9(6):445-50 [10981649.001]

[Cites] J Exp Med. 2000 Oct 2;192(7):1027-34 [11015443.001]

[Cites] Genes Immun. 2007 Jun;8(4):279-87 [17344889.001]

[Cites] Immunity. 2007 Jul;27(1):111-22 [17629517.001]

[Cites] J Virol. 2007 Sep;81(17):9249-58 [17567698.001]

[Cites] Rheumatology (Oxford). 2007 Sep;46(9):1492-4 [17673480.001]

[Cites] Mol Immunol. 2008 Jan;45(1):259-65 [17570528.001]

[Cites] Clin Exp Immunol. 2008 Jan;151(1):86-93 [18005363.001]

[Cites] Arthritis Rheum. 2007 Dec 15;57(8):1530-8 [18050226.001]

[Cites] Nat Immunol. 2001 Mar;2(3):261-8 [11224527.001]

[Cites] Science. 2001 Nov 16;294(5546):1540-3 [11711679.001]

[Cites] Nat Med. 2002 Aug;8(8):793-800 [12091876.001]

[Cites] Nat Genet. 2002 Dec;32(4):666-9 [12402038.001]

[Cites] J Immunol. 2003 Feb 1;170(3):1257-66 [12538684.001]

[Cites] Blood. 2003 Apr 1;101(7):2514-20 [12468426.001]

[Cites] Eur J Immunol. 2003 Oct;33(10):2706-16 [14515254.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Jul 20;101(29):10691-6 [15249675.001]

[Cites] Arthritis Rheum. 2004 Aug;50(8):2590-7 [15334473.001]

[Cites] Proc Natl Acad Sci U S A. 1978 Jul;75(7):3464-8 [150602.001]

[Cites] Arthritis Rheum. 1997 Sep;40(9):1725 [9324032.001]

[Cites] J Exp Med. 1998 Oct 5;188(7):1359-68 [9763615.001]

[Cites] J Immunol. 1998 Oct 15;161(8):3966-73 [9780165.001]

[Cites] Scand J Immunol. 1999 Jan;49(1):82-7 [10023862.001]

[Cites] Immunity. 1999 Aug;11(2):141-51 [10485649.001]

[Cites] Eur Cytokine Netw. 2004 Jul-Sep;15(3):222-30 [15542447.001]

[Cites] J Immunol. 2005 Feb 15;174(4):1888-97 [15699115.001]

[Cites] Nat Immunol. 2005 Mar;6(3):280-6 [15685176.001]

[Cites] J Immunol. 2005 Sep 1;175(5):3417-23 [16116236.001]

[Cites] J Immunol. 2006 Mar 15;176(6):3480-9 [16517716.001]

[Cites] J Leukoc Biol. 2006 Apr;79(4):686-95 [16461745.001]

[Cites] J Exp Med. 2006 Apr 17;203(4):883-95 [16606670.001]

[Cites] Br J Ophthalmol. 2006 Aug;90(8):1040-5 [16613922.001]

[Cites] Rheumatology (Oxford). 2006 Sep;45(9):1087-95 [16527880.001]

[Cites] J Immunol. 2006 Sep 15;177(6):3606-14 [16951320.001]

[Cites] J Immunol. 2006 Sep 15;177(6):4196-202 [16951385.001]

[Cites] Diabet Med. 2006 Oct;23(10):1145-50 [16978382.001]

[Cites] Arthritis Rheum. 2006 Sep;54(9):2951-62 [16947629.001]

[Cites] J Autoimmun. 2006 Sep;27(2):110-8 [16890406.001]

[Cites] J Viral Hepat. 2006 Nov;13(11):725-33 [17052271.001]

[Cites] J Immunol. 2006 Nov 1;177(9):5878-89 [17056512.001]

[Cites] J Clin Immunol. 2006 Nov;26(6):506-11 [17024563.001]

[Cites] J Exp Med. 2006 Nov 27;203(12):2737-47 [17116737.001]

[Cites] J Immunol. 2006 Dec 15;177(12):8291-5 [17142723.001]

[Cites] J Neuroimmunol. 2007 Jan;182(1-2):124-34 [17182110.001]

[Cites] J Immunol. 2007 Feb 15;178(4):2579-88 [17277168.001]

[Cites] Nat Immunol. 2007 Mar;8(3):239-45 [17304234.001]

[Cites] Eur J Hum Genet. 2007 Mar;15(3):336-41 [17228327.001]

[Cites] J Rheumatol. 2007 Apr;34(4):721-5 [17343323.001]

[Cites] Immunobiology. 2007;212(3):159-65 [17412283.001]

(PMID = 18650228.001).

[ISSN] 1462-0332

[Journal-full-title] Rheumatology (Oxford, England)

[ISO-abbreviation] Rheumatology (Oxford)

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / M01 RR000037; United States / NIAMS NIH HHS / AR / T32 AR007108; United States / NCRR NIH HHS / RR / M01-RR-00037

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human

[Other-IDs] NLM/ PMC2722808

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.

The Apc(MIN/+) mouse is a well-characterised model of intestinal tumourigenesis in which animals develop macroscopically detectable adenomas.

However, most of the adenomas are formed in the small intestine and resolution of events in the colon, the most relevant site for human disease, is limited.

Inducing colitis with dextran sodium sulphate (DSS) can selectively enhance the development of lesions in the colon.

We demonstrated that a DSS pre-treatment is well tolerated and effective at inducing colon adenomas in an Apc(MIN/+) mouse model.

We then investigated the effect of inhibiting vascular endothelial growth factor (VEGFR)- and epidermal growth factor receptor (EGFR)-dependent signalling pathways on the development of adenomas induced in DSS-pretreated (DSS/Apc(MIN/+)) or non-DSS-pretreated (Apc(MIN/+)) mice using vandetanib (ZD6474), a potent and selective inhibitor of VEGFR and EGFR tyrosine kinase activity.

Eight-week old Apc(MIN/+) mice were given either drinking water or 1.8% DSS and then vandetanib (ZD6474) (50 mg/kg/day) or vehicle by oral gavage for 28 days and sacrificed 24 h after the last dose and assessed for adenoma formation in the intestines.

DSS pre-treatment was well tolerated and significantly enhanced formation of adenomas in the colon of control Apc(MIN/+) mice.

Vandetanib treatment significantly reduced adenoma formation in the small intestine by 68% (P=0.001) and the colon by 77% (from 13.8 to 3.1, P=0.01) of DSS-pretreated Apc(MIN/+) mice.

In the Apc(MIN/+) group, vandetanib also reduced the mean number of adenomas in the small intestine by 76% (P<0.001) and in the colon by 60% (from 3.9 to 1.5, P=0.1).

DSS-pre-treatment increased the resolution of the model, allowing us to confirm statistically significant effects of vandetanib on the development and growth of colon adenomas in the Apc(MIN/+) mouse.

Moreover these preclinical data provide a rationale for studying the effects of vandetanib in early stages of intestinal cancer in the clinic.

[MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / pharmacology. Colitis / chemically induced. Colonic Neoplasms / prevention & control. Dextran Sulfate. Genes, APC. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology

[MeSH-minor] Animals. Disease Models, Animal. Intestine, Small / drug effects. Intestine, Small / enzymology. Intestine, Small / pathology. Mice. Mice, Inbred C57BL. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / metabolism. beta Catenin / metabolism

COS Scholar Universe. author profiles.

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20811697.001).

[ISSN] 1791-2423

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

[Grant] United Kingdom / Cancer Research UK / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 2.7.10.1 / EGFR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Pathways of the molecular pathogenesis of colorectal carcinoma have been extensively studied and molecular lesions during the development of the disease have been revealed.

High up in the list of colorectal cancer lesions are APC (adenomatous polyposis coli), K-ras, Smad4 (or DPC4-deleted in pancreatic cancer 4) and p53 genes.

The ubiquitin-proteasome system (UPS) is comprised of a multi-unit cellular protease system that regulates several dozens of cell proteins after their ligation with the protein ubiquitin.

Given that among these proteins are regulators of the cell cycle, apoptosis, angiogenesis, adhesion and cell signalling, this system plays a significant role in cell fate and carcinogenesis.

UPS inhibition has been found to be a pre-requisite for apoptosis and is already clinically exploited with the proteasome inhibitor bortezomib in multiple myeloma.

Inhibition of Cox-2 by aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been found to inhibit proliferation of colorectal cancer cells and in epidemiologic studies has been shown to reduce colon polyp formation in genetically predisposed populations and in the general population.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17488476.001).

[ISSN] 1582-1838

[Journal-full-title] Journal of cellular and molecular medicine

[ISO-abbreviation] J. Cell. Mol. Med.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Romania

[Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Ubiquitin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.25.1 / Proteasome Endopeptidase Complex

[Number-of-references] 298

[Other-IDs] NLM/ PMC3822826

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Expression of endothelial protein C receptor in tumor cell lines and It's significance].

AIM: To detect the role of activated protein C(APC) on proliferation of endothelial cell and investigate the expression of endothelial protein C receptor( EPCR) in variety of tumor cell lines.

METHODS: The effect of APC on endotheliocyte proliferation was determined by MTT colorimetry.

RESULTS: APC can increase the proliferation of EC significantly.

CONCLUSION: APC can stimulate the proliferation of endothelial cell.

High expression of EPCR in tumor cell lines provides a potential biological marker for malignancies.

[MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Interleukin-6 / metabolism. Interleukin-8 / metabolism. Protein C / metabolism

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20619102.001).

[ISSN] 1007-8738

[Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology

[ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD; 0 / Interleukin-6; 0 / Interleukin-8; 0 / PROCR protein, human; 0 / Protein C; 0 / Receptors, Cell Surface

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cutting edge: IFN-gamma enables APC to promote memory Th17 and abate Th1 cell development.

However, Th1, Th17, and memory but not naive T cells are colocalized in an inflammatory environment.

We show that IFN-gamma stimulates B7-H1 expression on APC subsets and abates their Th1 polarization capacity in a B7-H1-dependent manner.

Interestingly, IFN-gamma triggers APCs to produce IL-1 and IL-23 and enables them to induce memory Th17 expansion via IL-1 and IL-23 in a B7-H1-independent manner.

We propose a novel dynamic between Th1 and Th17 in the course of inflammation as follows: Th1-mediated inflammation is attenuated by IFN-gamma-induced B7-H1 on APCs and is evolved toward Th17-mediated chronic inflammation by IFN-gamma-induced, APC-derived IL-1 and IL-23.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18941172.001).

[ISSN] 1550-6606

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA099985; United States / NCI NIH HHS / CA / CA123088

[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 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human; 0 / Growth Inhibitors; 0 / Interleukin-1; 0 / Interleukin-17; 0 / Interleukin-23; 82115-62-6 / Interferon-gamma

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Elevated Dnmt3a activity promotes polyposis in Apc(Min) mice by relaxing extracellular restraints on Wnt signaling.

Here we use knock-in transgenic mice to investigate the consequences of intestinal epithelium-specific overexpression of de novo Dnmt3a.

METHODS: A novel gene targeting strategy, based on the intestinal epithelium-specific, uniform expression of the A33 glycoprotein, is employed to restrict Dnmt3a overexpression in homozygous A33(Dnmt3a) mutant mice.

RESULTS: A33(Dnmt3a) mice infrequently develop spontaneous intestinal polyps.

However, when genetically challenged, tumor multiplicity in A33(Dnmt3a);Apc(Min) compound mice is 3-fold higher than in Apc(Min) mice.

Although we observe a requirement for spontaneous loss of heterozygosity of the adenomatous polyposis coli (Apc) gene to trigger tumorigenesis in Apc(Min) mice, lesions in A33(Dnmt3a);Apc(Min) mice frequently retain the wild-type Apc allele.

However, epithelia from normal mucosa and polyps of A33(Dnmt3a);Apc(Min) mice show hypermethylation-mediated transcriptional silencing of the Wnt antagonists Sfrp5, and to a lesser extent, Sfrp1 and increased nuclear beta-catenin alongside activation of the Wnt-target gene Axin2/Conductin.

Conversely, enforced Sfrp5 expression suppresses canonical Wnt-signaling more effectively in wild-type than in Apc(Min) cells.

CONCLUSIONS: Aberrant activation of the canonical Wnt pathway, either by mono-allelic Apc loss or transcriptional silencing of Sfrp5 is largely insufficient to promote polyposis, but epistatic interactions between these genetic and epigenetic events enables initiation and promotion of disease.

[MeSH-major] Adenomatous Polyposis Coli / metabolism. DNA (Cytosine-5-)-Methyltransferase / metabolism. Genes, APC. Intestinal Mucosa / metabolism. Signal Transduction. Wnt Proteins / metabolism

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19454286.001).

[ISSN] 1528-0012

[Journal-full-title] Gastroenterology

[ISO-abbreviation] Gastroenterology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Gpa33 protein, mouse; 0 / Membrane Glycoproteins; 0 / Wnt Proteins; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] UbcH10 has a rate-limiting role in G1 phase but might not act in the spindle checkpoint or as part of an autonomous oscillator.

Ubiquitin-dependent proteolysis mediated by the anaphase-promoting complex/cyclosome (APC/C) ubiquitin ligase lies at the heart of the cell cycle.

The APC/C targets mitotic cyclins for destruction in mitosis and G1 phase and is then inactivated at S phase, thereby generating the alternating states of high and low cyclin-Cdk activity required for the alternation of mitosis and DNA replication.

Two key questions are how the APC/C is held in check by the spindle-assembly checkpoint to delay cells in mitosis in the presence of improperly attached chromosomes, and how the APC/C is inactivated once cells exit mitosis.

The ubiquitin-conjugating protein UbcH10 has been proposed to be crucial in the answers to both questions.

However, here we show that the behaviour of UbcH10 is inconsistent with both a crucial role in the spindle checkpoint and in inactivating the APC/C as part of an autonomous oscillator.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18559889.001).

[ISSN] 0021-9533

[Journal-full-title] Journal of cell science

[ISO-abbreviation] J. Cell. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Cyclin A; EC 6.3.2.19 / UBE2C protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis.

Transthyretin (TTR) tetramer dissociation, misfolding and misassembly are required for the process of amyloid fibril formation associated with familial amyloid polyneuropathy (FAP).

Here, we investigated the feasibility of using these molecules for the treatment of FAP utilizing serum samples from 37 FAP patients with 10 different mutations.

We demonstrated that the TTR heterotetramer structures in FAP patients serum are significantly less stable than that in normal subjects, indicating the instability of the variant TTR structure is a fundamental cause of TTR amyloidosis.

Trivalent chromium at levels obtained by oral supplementation did not stabilize TTR in a statistically significant fashion.

Importantly, diflunisal increased serum TTR stability in FAP patients beyond the level of normal controls.

[MeSH-major] Amyloid Neuropathies, Familial / metabolism. Amyloid beta-Peptides / biosynthesis. Amyloid beta-Peptides / genetics. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Diflunisal / pharmacology. Prealbumin / biosynthesis. Prealbumin / genetics

[MeSH-minor] Adult. Aged. Chromium / pharmacology. Female. Flufenamic Acid / pharmacology. Humans. Hydrogen-Ion Concentration. Iron / physiology. Male. Middle Aged. Mutation / physiology. Protein Denaturation

Genetic Alliance. consumer health - Familial Amyloid Polyneuropathy.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. IRON, ELEMENTAL .

Hazardous Substances Data Bank. CHROMIUM, ELEMENTAL .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17028027.001).

[ISSN] 0168-0102

[Journal-full-title] Neuroscience research

[ISO-abbreviation] Neurosci. Res.

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / DK046335

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Prealbumin; 0R0008Q3JB / Chromium; 60GCX7Y6BH / Flufenamic Acid; 7C546U4DEN / Diflunisal; E1UOL152H7 / Iron

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Mycobacterium avium ssp. paratuberculosis recombinant heat shock protein 70 interaction with different bovine antigen-presenting cells.

Abstract Heat shock proteins (Hsp) can deliver antigen into the major histocompatibility complex class I presentation pathway of antigen-presenting cells (APC), a process called cross priming, thus stimulating antigen-specific CD8+ T-cell reactions.

Hsp were shown to elicit proinflammatory responses in APC.

Both processes require interaction of Hsp with APC via specific receptors.

Characterized monocyte-derived macrophages, monocyte-derived dendritic cells (DC) and BoMac, an immortalized bovine macrophage cell line, were used to investigate the interaction of rHsp70 with different bovine APC.

Involvement of CD91 as a cellular receptor for rHsp70 was demonstrated; however, competition studies with immature DC demonstrated that other receptors exist on bovine APC.

[MeSH-major] Antigen-Presenting Cells / immunology. Bacterial Proteins / immunology. HSP70 Heat-Shock Proteins / immunology. Mycobacterium avium subsp. paratuberculosis / immunology

antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15787741.001).

[ISSN] 0300-9475

[Journal-full-title] Scandinavian journal of immunology

[ISO-abbreviation] Scand. J. Immunol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD14; 0 / Bacterial Proteins; 0 / Bacterial Vaccines; 0 / HSP70 Heat-Shock Proteins; 0 / alpha-Macroglobulins

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A rapid and sensitive prenatal diagnosis of familial amyloidotic polyneuropathy ATTR Val30Met by mass spectrometry.

OBJECTIVE: To make a prenatal diagnosis of familial amyloidotic polyneuropathy (FAP) by mass spectrometry with the amniotic fluid.

METHODS: Amniotic-fluid samples of three non-FAP pregnant women and six amniotic-fluid samples of fetal mice whose mother was a heterozygotic FAP amyloidgenic transthyretin (ATTR) Val30Met gene carrier were collected.

CONCLUSION: Mass spectrometry analysis of the amniotic fluid might be a useful tool to make a prenatal diagnosis of FAP ATTR Val30Met.

[MeSH-major] Amyloid Neuropathies, Familial / diagnosis. Mass Spectrometry / methods. Prealbumin / analysis. Prenatal Diagnosis / methods

MedlinePlus Health Information. consumer health - Prenatal Testing.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. (L)-Methionine .

Hazardous Substances Data Bank. L-Valine .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19609897.001).

[ISSN] 1097-0223

[Journal-full-title] Prenatal diagnosis

[ISO-abbreviation] Prenat. Diagn.

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies; 0 / Prealbumin; AE28F7PNPL / Methionine; HG18B9YRS7 / Valine

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Achieving routine sub 30 minute door-to-balloon times in a high volume 24/7 primary angioplasty center with autonomous ambulance diagnosis and immediate catheter laboratory access.

Using autonomous ambulance diagnosis with open access to the myocardial infarction center catheter laboratory, we compared reperfusion times and clinical outcomes for the final 2 years of TL with the first 3 years of PPCI.

RESULTS: Comparison was made between TL (2002-2004, n = 185) and PPCI (2004-2007, n = 704); all times are medians in minutes (interquartile range): for TL, symptom to needle 153 (85-225), call to needle 58 (49-73), first professional contact (FPC) to needle 47 (39-63), door to needle 18 (12-30) (mortality: 7.6% at 30 days, 9.2% at 1 year); for interhospital transfer PPCI (n = 227), symptom to balloon 226 (175-350), call to balloon 135 (117-188), FPC to balloon 121 (102-166), first door-to-balloon 100 (80-142) (mortality: 7.0% at 30 days, 12.3% at 1 year); for direct-access PPCI (n = 477), symptom to balloon 142 (101-238), call to balloon 79 (70-93), FPC to balloon 69 (59-82), door to balloon 20 (16-29) (mortality: 4.6% at 30 days, 8.6% at 1 year).

With autonomous ambulance diagnosis and open access direct to the catheter laboratory, a median door-to-balloon time of <30 minutes day and night was achieved, and >95% of patients were reperfused within 1 hour.

MedlinePlus Health Information. consumer health - Heart Attack.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[ErratumIn] Am Heart J. 2010 Feb;159(2):330

(PMID = 19853705.001).

[ISSN] 1097-6744

[Journal-full-title] American heart journal

[ISO-abbreviation] Am. Heart J.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Fibrinolytic Agents

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We demonstrated that LAB induced strong TLR2-expressing APC responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood).

LAB and HRV have an additive effect on TLR2- and TLR9-expressing APC responses, consistent with the adjuvant effect of LAB.

LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14- APC responses in spleen and the serum IFN-alpha response induced by HRV.

MedlinePlus Health Information. consumer health - Rotavirus Infections.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Clin Immunol. 2008 Sep;128(3):400-8 [18565796.001]

[Cites] Antonie Van Leeuwenhoek. 1999 Jul-Nov;76(1-4):383-9 [10532394.001]

[Cites] Dig Dis Sci. 1999 Oct;44(10):2119-23 [10548366.001]

[Cites] Immunology. 2001 Apr;102(4):396-404 [11328373.001]

[Cites] Immunology. 2001 Oct;104(2):175-84 [11683958.001]

[Cites] Vet Immunol Immunopathol. 2002 Sep 10;87(3-4):147-60 [12072229.001]

[Cites] Ann Allergy Asthma Immunol. 2002 Jun;88(6):543-7; quiz 548-50, 583 [12086359.001]

[Cites] Antonie Van Leeuwenhoek. 2002 Aug;82(1-4):341-52 [12369201.001]

[Cites] Vet Immunol Immunopathol. 2003 Jan 10;91(1):1-12 [12507844.001]

[Cites] Science. 2003 Aug 1;301(5633):640-3 [12855817.001]

[Cites] J Immunol. 2003 Sep 15;171(6):3154-62 [12960343.001]

[Cites] Immunology. 2003 Dec;110(4):440-9 [14632641.001]

[Cites] Gastroenterology. 2004 Feb;126(2):520-8 [14762789.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3516-21 [14993594.001]

[Cites] Nat Rev Immunol. 2004 Jul;4(7):499-511 [15229469.001]

[Cites] J Clin Microbiol. 1982 Feb;15(2):312-9 [6279693.001]

[Cites] Am J Vet Res. 1986 Aug;47(8):1697-703 [3019187.001]

[Cites] Pediatr Res. 1992 Aug;32(2):141-4 [1324462.001]

[Cites] Lancet. 1994 Oct 15;344(8929):1046-9 [7934445.001]

[Cites] FEMS Immunol Med Microbiol. 1994 Nov;10(1):55-63 [7874079.001]

[Cites] J Pediatr Gastroenterol Nutr. 1995 Apr;20(3):333-8 [7608829.001]

[Cites] Vaccine. 1995 Feb;13(3):310-2 [7631519.001]

[Cites] J Virol. 1996 May;70(5):3075-83 [8627786.001]

[Cites] J Gen Virol. 1996 Jul;77 ( Pt 7):1431-41 [8757984.001]

[Cites] Arch Virol Suppl. 1996;12:153-61 [9015112.001]

[Cites] Pediatr Infect Dis J. 1997 Dec;16(12):1103-7 [9427453.001]

[Cites] Clin Exp Immunol. 1999 May;116(2):283-90 [10337020.001]

[Cites] Appl Microbiol. 1964 Jul;12:295-300 [14199016.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):3906-12 [15671160.001]

[Cites] J Virol. 2005 May;79(9):5428-36 [15827157.001]

[Cites] Eur J Nutr. 2005 Oct;44(7):406-13 [15578195.001]

[Cites] J Virol. 2006 Jan;80(1):372-82 [16352562.001]

[Cites] Folia Biol (Praha). 2005;51(6):188-97 [16419614.001]

[Cites] Clin Vaccine Immunol. 2006 Feb;13(2):219-26 [16467329.001]

[Cites] Cell Res. 2006 Feb;16(2):141-7 [16474426.001]

[Cites] Immunity. 2006 Feb;24(2):153-63 [16473828.001]

[Cites] Emerg Infect Dis. 2006 Feb;12(2):304-6 [16494759.001]

[Cites] J Gastroenterol Hepatol. 2006 Mar;21(3):521-30 [16638093.001]

[Cites] J Allergy Clin Immunol. 2006 May;117(5):979-87; quiz 988 [16675322.001]

[Cites] Aliment Pharmacol Ther. 2006 Jun 1;23(11):1567-74 [16696804.001]

[Cites] Clin Exp Immunol. 2006 Jun;144(3):376-81 [16734605.001]

[Cites] Vet Res. 2006 Nov-Dec;37(6):791-812 [16973119.001]

[Cites] Curr Opin Gastroenterol. 2007 Jan;23(1):39-43 [17133083.001]

[Cites] Vet Immunol Immunopathol. 2007 Feb 15;115(3-4):309-19 [17178162.001]

[Cites] Nutrition. 2007 Mar;23(3):254-60 [17352961.001]

[Cites] J Immunol. 2007 Apr 1;178(7):4548-56 [17372013.001]

[Cites] Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2007 Mar;21(1):38-40 [17429531.001]

[Cites] Immunol Invest. 2007;36(4):413-21 [17691023.001]

[Cites] J Gastroenterol Hepatol. 2007 Oct;22(10):1627-32 [17845690.001]

[Cites] J Gen Virol. 2007 Oct;88(Pt 10):2749-61 [17872528.001]

[Cites] J Anim Sci. 2007 Dec;85(12):3256-66 [17785595.001]

[Cites] Acta Pharmacol Sin. 2008 Feb;29(2):239-44 [18215354.001]

[Cites] Vet Immunol Immunopathol. 2008 Feb 15;121(3-4):222-31 [18006076.001]

[Cites] Vet Immunol Immunopathol. 2008 Mar 15;122(1-2):175-81 [18023882.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):2993-8 [18287072.001]

[Cites] AIDS. 2008 Mar 30;22(6):685-94 [18356597.001]

[Cites] Asia Pac J Clin Nutr. 2008;17(1):30-4 [18364323.001]

[Cites] PLoS Negl Trop Dis. 2008;2(4):e215 [18398488.001]

[Cites] PLoS Pathog. 2008 Jun;4(6):e1000079 [18535658.001]

[Cites] Vaccine. 2008 Jul 4;26(29-30):3655-61 [18524434.001]

(PMID = 19054578.001).

[ISSN] 0165-2427

[Journal-full-title] Veterinary immunology and immunopathology

[ISO-abbreviation] Vet. Immunol. Immunopathol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / R01 AI033561-11; United States / NIAID NIH HHS / AI / R01 AI033561; United States / NCCIH NIH HHS / AT / R21 AT002524-02; United States / NCCIH NIH HHS / AT / R21 AT002524; United States / NIAID NIH HHS / AI / AI033561-11; United States / NCCIH NIH HHS / AT / 1R21AT002524; United States / NIAID NIH HHS / AI / R01AI033561

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Cytokines; 0 / Toll-Like Receptors

[Other-IDs] NLM/ NIHMS89734; NLM/ PMC2653198

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Nowadays, patients with ulcerative colitis or familial adenomatous polyposis of the colon undergo proctocolectomy as the definitive treatment for their underlying disease.

This contribution describes the surgical indications and pathophysiological changes for the colon J-pouch and ileoanal reservoir.

In addition, explanations of the surgical techniques for both procedures are presented.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Dis Colon Rectum. 1999 Jul;42(7):896-902 [10411436.001]

[Cites] Ann Surg. 1986 Oct;204(4):375-83 [3767475.001]

[Cites] Ann Surg. 2002 Feb;235(2):207-16 [11807360.001]

[Cites] Br J Surg. 1996 Jul;83(7):978-80 [8813791.001]

[Cites] Int J Colorectal Dis. 1998;13(4):160-3 [9810519.001]

[Cites] Chirurg. 1993 Aug;64(8):601-13 [8404287.001]

[Cites] Int J Colorectal Dis. 1998;13(4):151-3 [9810516.001]

[Cites] Br J Surg. 1997 Oct;84(10):1437-41 [9361608.001]

[Cites] Dis Colon Rectum. 2001 Jan;44(1):37-42 [11805561.001]

[Cites] Dis Colon Rectum. 2002 May;45(5):660-7 [12004217.001]

[Cites] Dis Colon Rectum. 1998 Jul;41(7):817-22; discussion 822-3 [9678365.001]

[Cites] Dis Colon Rectum. 2001 Apr;44(4):487-99 [11330575.001]

[Cites] Ann Surg. 2003 Aug;238(2):214-20 [12894014.001]

[Cites] Langenbecks Arch Surg. 2001 Apr;386(3):193-9 [11382321.001]

[Cites] Dis Colon Rectum. 1997 Jan;40(1):30-4 [9102258.001]

[Cites] Ann Surg. 2001 Dec;234(6):788-94 [11729385.001]

[Cites] Surg Today. 2002;32(6):487-92 [12107771.001]

[Cites] Int J Colorectal Dis. 2000 Apr;15(2):114-7 [10855555.001]

[Cites] Int J Colorectal Dis. 1998;13(5-6):241-6 [9870169.001]

[Cites] Ann Surg. 1995 Aug;222(2):120-7 [7639579.001]

[Cites] Ann Surg. 1999 Oct;230(4):575-84; discussion 584-6 [10522727.001]

[Cites] Zentralbl Chir. 1994;119(12):867-77 [7846969.001]

[Cites] Int J Colorectal Dis. 1999 Apr;14(2):114-8 [10367257.001]

[Cites] Int J Colorectal Dis. 1999 Nov;14 (4-5):237-44 [10647633.001]

[Cites] Int J Colorectal Dis. 1999 Aug;14(3):158-63 [10460907.001]

(PMID = 18210064.001).

[ISSN] 1433-0563

[Journal-full-title] Der Urologe. Ausg. A

[ISO-abbreviation] Urologe A

[Language] ger

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Germany

[Number-of-references] 40

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Dietary anthocyanin-rich tart cherry extract inhibits intestinal tumorigenesis in APC(Min) mice fed suboptimal levels of sulindac.

A promising approach for cancer chemoprevention might be a combination therapy utilizing dietary phytochemicals and anticarcinogenic pharmaceuticals at a suboptimal dosage to minimize any potential adverse side effects.

Mice that were fed anthocyanin-rich extract (at any dose) in combination with sulindac had fewer tumors and a smaller total tumor burden (total tumor area per mouse) in the small intestine when compared to mice fed sulindac alone.

These results suggest that a dietary combination of tart cherry anthocyanins and sulindac is more protective against colon cancer than sulindac alone.

[MeSH-major] Anthocyanins / administration & dosage. Antineoplastic Agents / administration & dosage. Fruit / chemistry. Intestinal Neoplasms / prevention & control. Prunus / chemistry. Sulindac / administration & dosage

[MeSH-minor] Adenomatous Polyposis Coli / genetics. Animals. Diet. Female. Male. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. Mutation. Plant Extracts / administration & dosage. Plant Extracts / chemistry

COS Scholar Universe. author profiles.

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17147414.001).

[ISSN] 0021-8561

[Journal-full-title] Journal of agricultural and food chemistry

[ISO-abbreviation] J. Agric. Food Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Anthocyanins; 0 / Antineoplastic Agents; 0 / Plant Extracts; 184SNS8VUH / Sulindac

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Immunization in familial amyloidotic polyneuropathy: counteracting deposition by immunization with a Y78F TTR mutant.

The mechanism of amyloid formation in familial amyloidotic polyneuropathy (FAP), a hereditary disorder associated with mutant transthyretin (TTR), is still unknown.

To test whether TTR deposition in FAP can be counteracted by antibodies for cryptic epitopes, we immunized with TTR Y78F, transgenic mice carrying the most common FAP-associated TTR mutant--V30M (transthyretin mutant with methionine replacing valine at position 30)--at selected ages that present normally with either nonfibrillar or TTR amyloid deposition.

Compared to age-matched control nonimmunized mice, Y78F-immunized mice had a significant reduction in TTR deposition usually found in this strain, in particular in stomach and intestine; by contrast, animals immunized with V30M did not show differences in deposition in comparison with nonimmunized mice.

Immunohistochemical analyses of tissues revealed that immunization with Y78F lead to infiltration by lymphocytes and macrophages at common deposition sites, but not in tissues such as liver, choroid plexus, and Langerhans islets, in which TTR is produced.

Therefore, TTR immunization with selected TTR mutants has potential application in immune therapy for FAP.

[MeSH-major] Amyloid Neuropathies, Familial / prevention & control. Mutation. Prealbumin / administration & dosage

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16357867.001).

[ISSN] 0023-6837

[Journal-full-title] Laboratory investigation; a journal of technical methods and pathology

[ISO-abbreviation] Lab. Invest.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Prealbumin

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

These differences are not mediated by a different interaction with RhoGDIs.

[MeSH-major] Cell Movement. Neoplasm Invasiveness. Pancreatic Neoplasms / pathology. rho GTP-Binding Proteins / metabolism. rhoA GTP-Binding Protein / metabolism

[MeSH-minor] Cell Line, Tumor. Deep Brain Stimulation. Humans. Protein Isoforms / chemistry. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. rap GTP-Binding Proteins / chemistry. rap GTP-Binding Proteins / genetics. rap GTP-Binding Proteins / metabolism

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19642867.001).

[ISSN] 1437-4315

[Journal-full-title] Biological chemistry

[ISO-abbreviation] Biol. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Protein Isoforms; 0 / RHOC protein, human; 0 / RNA, Messenger; EC 3.6.5.2 / rap GTP-Binding Proteins; EC 3.6.5.2 / rho GTP-Binding Proteins; EC 3.6.5.2 / rhoA GTP-Binding Protein

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Activation of EDTA-resistant gelatinases in malignant human tumors.

Among the many proteases associated with human cancer, seprase or fibroblast activation protein alpha, a type II transmembrane glycoprotein, has two types of EDTA-resistant protease activities: dipeptidyl peptidase and a 170-kDa gelatinase activity.

To test if activation of gelatinases associated with seprase could be involved in malignant tumors, we used a mammalian expression system to generate a soluble recombinant seprase (r-seprase).

Proteins purified from experimental xenografts and malignant tumors using antibody- or lectin-affinity columns in the presence of 5 mmol/L EDTA were assayed for seprase activation in vivo.

Seprase expression and activation occur most prevalently in ovarian carcinoma but were also detected in four other malignant tumor types, including adenocarcinoma of the colon and stomach, invasive ductal carcinoma of the breast, and malignant melanoma.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. Disodium EDTA .

Hazardous Substances Data Bank. ETHYLENEDIAMINE TETRAACETIC ACID .

Hazardous Substances Data Bank. DISODIUM CALCIUM EDTA .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Science. 2004 Oct 1;306(5693):108-11 [15459390.001]

[Cites] J Biol Chem. 2004 Aug 13;279(33):34691-7 [15175333.001]

[Cites] Proc Natl Acad Sci U S A. 1994 Jun 7;91(12):5657-61 [7911242.001]

[Cites] Int J Cancer. 1994 Aug 1;58(3):385-92 [7519584.001]

[Cites] Am J Pathol. 1995 May;146(5):1150-60 [7747809.001]

[Cites] J Biol Chem. 1997 Mar 21;272(12):7595-601 [9065413.001]

[Cites] Biochim Biophys Acta. 1997 Jul 10;1361(1):11-9 [9247085.001]

[Cites] Eur J Biochem. 1998 Jun 15;254(3):650-4 [9688278.001]

[Cites] Mod Pathol. 1998 Sep;11(9):855-63 [9758365.001]

[Cites] Hepatology. 1999 Jun;29(6):1768-78 [10347120.001]

[Cites] J Biol Chem. 1999 Aug 27;274(35):24947-52 [10455171.001]

[Cites] Oncology. 2004;67(5-6):411-9 [15713998.001]

[Cites] Mol Cancer Ther. 2005 Mar;4(3):351-60 [15767544.001]

[Cites] J Biol Chem. 2005 May 20;280(20):19441-4 [15809306.001]

[Cites] Cancer Lett. 2005 Sep 28;227(2):229-36 [16196122.001]

[Cites] Cancer Res. 1994 Nov 1;54(21):5702-10 [7923219.001]

[Cites] J Biol Chem. 1999 Dec 17;274(51):36505-12 [10593948.001]

[Cites] J Biol Chem. 2000 Jan 28;275(4):2554-9 [10644713.001]

[Cites] Int J Cancer. 2001 Jan 20;95(1):67-72 [11241314.001]

[Cites] J Biol Chem. 2002 Aug 9;277(32):29231-41 [12023964.001]

[Cites] Cancer Res. 2002 Aug 15;62(16):4767-72 [12183436.001]

[Cites] J Biol Chem. 1998 May 22;273(21):13366 [12755100.001]

[Cites] Anticancer Res. 2003 Jul-Aug;23(4):3195-8 [12926053.001]

[Cites] Oncology. 2003;65(4):363-70 [14707457.001]

[Cites] Cancer Res. 2004 Apr 15;64(8):2712-6 [15087384.001]

[Cites] Oncogene. 2004 Jul 15;23(32):5435-46 [15133496.001]

[Cites] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8296-300 [2172980.001]

(PMID = 17047060.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA039077; United States / NIBIB NIH HHS / EB / R01EB002065; United States / NIBIB NIH HHS / EB / R01 EB002065; United States / NCRR NIH HHS / RR / M01 RR010710; United States / NCRR NIH HHS / RR / M01RR10710; United States / NCI NIH HHS / CA / R01CA0039077

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Membrane Proteins; 0 / Recombinant Proteins; 9G34HU7RV0 / Edetic Acid; EC 3.4.14.- / Dipeptidyl-Peptidases and Tripeptidyl-Peptidases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases

[Other-IDs] NLM/ NIHMS11890; NLM/ PMC1626657

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The binding of 2,4-dinitrophenol to wild-type and amyloidogenic transthyretin.

Systemic deposition of transthyretin (TTR) amyloid fibrils is always observed in familial amyloidotic polyneuropathy, senile systemic amyloidosis and familial amyloidotic cardiomyopathy patients.

The destabilization of a native protein with consequent conformational changes appears to be a common link in several human amyloid diseases.

Intensive research has been directed towards finding small molecules that could work as therapeutic agents for the prevention/inhibition of amyloid diseases through stabilization of the native fold of the potentially amyloidogenic protein.

This work provides insight into the structural determinants of the highly stabilizing effects of 2,4-dinitrophenol on wild-type TTR.

As a result of 2,4-dinitrophenol binding, the two dimers in the TTR tetramer become closer, increasing the stability of the protein.

MedlinePlus Health Information. consumer health - Amyloidosis.

Hazardous Substances Data Bank. 2,4-Dinitrophenol .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16627944.001).

[ISSN] 0907-4449

[Journal-full-title] Acta crystallographica. Section D, Biological crystallography

[ISO-abbreviation] Acta Crystallogr. D Biol. Crystallogr.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] 0 / Peptides; 0 / Prealbumin; Q13SKS21MN / 2,4-Dinitrophenol

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Onset of liver metastasis after histologically curative resection of pancreatic cancer.

PURPOSE: We assessed the possibility of predicting the time of onset of liver metastases by measuring the postoperative changes in serum carbohydrate antigen (CA)19-9 after curative resection of pancreatic cancers.

METHODS: Among 28 patients who underwent histologically defined curative resection of pancreatic cancer between 1984 and 1999, liver metastasis developed in 11 patients with elevated serum CA19-9 levels.

We plotted the serum CA19-9 levels against time on a semilogarithmic graph.

Over the linear part of the curve, the time when log[CA19-9] equaled zero was defined as the time of onset of liver metastases.

The log[CA19-9] level doubling time was then calculated and evaluated in relation to the survival period.

RESULTS: The serum CA19-9 levels increased linearly in 10 of the 11 patients.

The predicted time of onset of liver metastasis ranged from preoperative day 163.0 to postoperative day 27.1, being preoperative in eight patients.

The doubling time until death correlated strongly with survival in the eight patients with maintained log[CA19-9] linearity.

CONCLUSION: The onset of liver metastases might be preoperative in patients with advanced pancreatic cancer.

Therefore, neoadjuvant chemotherapy should be mandatory even if there is no sign of liver metastases.

[MeSH-major] Biomarkers, Tumor / blood. CA-19-9 Antigen / blood. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

[MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Prognosis. Time Factors

Genetic Alliance. consumer health - Liver cancer.

Genetic Alliance. consumer health - Pancreatic cancer.

MedlinePlus Health Information. consumer health - Liver Cancer.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Hepatogastroenterology. 1998 Jan-Feb;45(19):253-9 [9496523.001]

[Cites] J Gastrointest Surg. 1998 Jan-Feb;2(1):28-35 [9841965.001]

[Cites] Int J Pancreatol. 1995 Apr;17(2):139-46 [7622937.001]

[Cites] Int J Biol Markers. 1999 Apr-Jun;14(2):99-105 [10399629.001]

[Cites] Ann Surg Oncol. 1997 Oct-Nov;4(7):551-6 [9367020.001]

[Cites] Int J Pancreatol. 1990 Aug-Nov;7(1-3):201-7 [1964472.001]

[Cites] Am J Surg. 1978 Sep;136(3):322-7 [707698.001]

[Cites] Int J Radiat Oncol Biol Phys. 1999 Jul 15;44(5):1039-46 [10421536.001]

[Cites] Int J Biol Markers. 1994;9(1):33-7 [8051433.001]

[Cites] Cancer. 1987 Nov 15;60(10):2428-31 [3478117.001]

[Cites] Anticancer Res. 1999 Jul-Aug;19(4A):2433-5 [10470171.001]

[Cites] J Surg Oncol. 1993 Mar;52(3):137-41 [8441267.001]

[Cites] HPB Surg. 1994;8(2):107-10 [7880768.001]

[Cites] Hepatogastroenterology. 1996 May-Jun;43(9):748-55 [8799425.001]

[Cites] Nihon Geka Gakkai Zasshi. 1991 Sep;92(9):1074-7 [1944157.001]

(PMID = 16493535.001).

[ISSN] 0941-1291

[Journal-full-title] Surgery today

[ISO-abbreviation] Surg. Today

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A novel mutation (g2172-->c) in the factor V gene in a Chinese family with hereditary activated protein C resistance.

BACKGROUND: Activated protein C resistance (APC-R) was a major risk factor for venous thromboembolism(VTE) in Caucasians, and at least 90% of APC-R were associated with the point mutation of factor V (FV) gene (Arg506-->Gln, FV Leiden).

OBJECTIVE: To identify the genetic defect of FV in a Chinese family with APC-R associated with VTE.

Blood samples were obtained from five family members (including the proband) for screening APC-R by coagulation assay and the genetic defect of FV using direct sequencing.

RESULTS: Four out of five members had APC-R.

We identified a novel mutation (G2172-->C) in exon 13 of the FV gene, which was present in all the individuals with APC-R but was absent in the individual without APC-R.

This mutation is predicted to result in the replacement of glutamate by aspartate at position 666, close to one of the APC cleavage sites.

CONCLUSIONS: We have identified, for the first time, a novel mutation (G2172-->C) of FV that was associated with APC-R in a Chinese family with VTE.

We speculate that this mutation interferes with cleavage at Arg679 by APC.

[MeSH-major] Activated Protein C Resistance / genetics. Factor V / genetics. Point Mutation

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.

(PMID = 20304467.001).

[ISSN] 1879-2472

[Journal-full-title] Thrombosis research

[ISO-abbreviation] Thromb. Res.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 9001-24-5 / Factor V

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Currently, the most effective strategy available for colon cancer prevention is endoscopic screening, with polypectomy or surgical resection for advanced lesions.

Data obtained from animal and epidemiological studies and most recently from randomised, placebo controlled trials, suggest that non-steroidal anti-inflammatory drugs may prove effective chemopreventive agents in different groups of people, from patients with familial adenomatous polyposis to those with sporadic adenomas.

[MeSH-minor] Colorectal Neoplasms, Hereditary Nonpolyposis / prevention & control. Humans. Randomized Controlled Trials as Topic. Treatment Outcome

Genetic Alliance. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Science. 1992 May 1;256(5057):668-70 [1350108.001]

[Cites] Gut. 2002 Jun;50(6):857-60 [12010890.001]

[Cites] J Natl Cancer Inst. 1993 Jun 2;85(11):875-84 [8492316.001]

[Cites] J Natl Cancer Inst. 1993 Aug 4;85(15):1220-4 [8331682.001]

[Cites] Br J Surg. 1993 Dec;80(12):1618-9 [8298943.001]

[Cites] Ann Intern Med. 1994 Aug 15;121(4):241-6 [8037405.001]

[Cites] Cancer Res. 1994 Nov 15;54(22):5953-8 [7954428.001]

[Cites] Lancet. 1995 Apr 1;345(8953):855-6 [7898240.001]

[Cites] Cancer Res. 1995 Jun 15;55(12):2556-9 [7780968.001]

[Cites] N Engl J Med. 1995 Sep 7;333(10):609-14 [7637720.001]

[Cites] Cancer Res. 1996 Oct 15;56(20):4566-9 [8840961.001]

[Cites] Cell. 1996 Nov 29;87(5):803-9 [8945508.001]

[Cites] Blood. 2002 Aug 15;100(4):1493-5 [12149237.001]

[Cites] CA Cancer J Clin. 2003 Jan-Feb;53(1):5-26 [12568441.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):879-80 [12621130.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):919-32 [12621137.001]

[Cites] Trends Neurosci. 2003 Apr;26(4):207-14 [12689772.001]

[Cites] Arch Neurol. 2003 Dec;60(12):1685-91 [14676042.001]

[Cites] Neurology. 2004 Jul 13;63(1):33-9 [15249607.001]

[Cites] Nat New Biol. 1971 Jun 23;231(25):232-5 [5284360.001]

[Cites] Gut. 1982 Oct;23(10):835-42 [7117903.001]

[Cites] Science. 1990 Jan 19;247(4940):322-4 [2296722.001]

[Cites] J Biol Chem. 1991 Jul 15;266(20):12866-72 [1712772.001]

[Cites] Gastroenterology. 1991 Sep;101(3):635-9 [1650315.001]

[Cites] N Engl J Med. 1991 Dec 5;325(23):1593-6 [1669840.001]

[Cites] Proc Natl Acad Sci U S A. 1992 May 1;89(9):3917-21 [1570314.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3336-40 [9096394.001]

[Cites] Jpn J Cancer Res. 1997 Nov;88(11):1044-51 [9439679.001]

[Cites] Cancer Res. 1998 Feb 1;58(3):409-12 [9458081.001]

[Cites] Ann Intern Med. 1998 May 1;128(9):713-20 [9556464.001]

[Cites] Gastroenterology. 1999 Aug;117(2):350-8 [10419916.001]

[Cites] Cancer. 1999 Dec 1;86(11 Suppl):2551-63 [10630181.001]

[Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]

[Cites] N Engl J Med. 2000 Jun 29;342(26):1960-8 [10874065.001]

[Cites] N Engl J Med. 2000 Nov 23;343(21):1520-8, 2 p following 1528 [11087881.001]

[Cites] Cancer Res. 2001 Feb 15;61(4):1733-40 [11245490.001]

[Cites] Neuron. 2001 Jun;30(3):665-76 [11430801.001]

[Cites] Lancet Oncol. 2002 Mar;3(3):166-74 [11902503.001]

[Cites] N Engl J Med. 1993 May 6;328(18):1313-6 [8385741.001]

(PMID = 15811884.001).

[ISSN] 0032-5473

[Journal-full-title] Postgraduate medical journal

[ISO-abbreviation] Postgrad Med J

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents

[Other-IDs] NLM/ PMC1743256