[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 23 of about 23
1. Zhu CB, Steiner JA, Munn JL, Daws LC, Hewlett WA, Blakely RD: Rapid stimulation of presynaptic serotonin transport by A(3) adenosine receptors. J Pharmacol Exp Ther; 2007 Jul;322(1):332-40
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have demonstrated post-translational regulation of SERT mediated by multiple Ser/Thr kinases, including protein kinases C and G (PKC and PKG) and p38 mitogen-activated protein kinase (MAPK), as well as the Ser/Thr phosphatase PP2A.
  • Less well studied are specific surface receptors that target these signaling pathways to control SERT surface expression and/or catalytic rates.
  • Using rat basophilic leukemia 2H3 cell line (RBL-2H3), we previously established that activation of A(3) adenosine receptors (A(3)AR) stimulates SERT activity via both PKG and p38 MAPK (Zhu et al., 2004a).
  • Here we report that the A(3)AR agonist N(6)-(3-iodobenzyl)-N-methyl-5'carbamoyladenosine (IB-MECA) rapidly (10 min) and selectively stimulates 5-HT transport in mouse midbrain, hippocampal, and cortical synaptosomes.
  • Kinetic analyses demonstrate that IB-MECA induces an increase of 5-HT transport V(max) with no significant change in K(m).
  • As in RBL-2H3 cells, IB-MECA stimulation of synaptosomal 5-HT uptake can be blocked by preincubation with PKG antagonists N-[2-(methylamino)ethy]-5-isoquinoline-sulfonamide (H8) and DT-2 (YGRKKRRQRRRPPLRK(5)H), as well as by the p38 MAPK inhibitor SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole].
  • Together, these results identify a novel, region-specific action of CNS A(3)ARs in the modulation of SERT-mediated 5-HT transport that may be relevant for the etiology and/or therapy of 5-HT-linked brain disorders.
  • [MeSH-minor] Adenosine / analogs & derivatives. Adenosine / pharmacology. Adenosine-5'-(N-ethylcarboxamide) / pharmacology. Animals. Biological Transport. Cyclic GMP-Dependent Protein Kinases / physiology. MAP Kinase Signaling System. Male. Mice. Mice, Inbred C57BL. Rats. Rats, Sprague-Dawley. Serotonin Plasma Membrane Transport Proteins / physiology. Synaptosomes / metabolism. p38 Mitogen-Activated Protein Kinases / physiology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Adenosine .
  • 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 = 17460150.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA07390
  • [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 / Receptor, Adenosine A3; 0 / Serotonin Plasma Membrane Transport Proteins; 152918-18-8 / N(6)-(3-iodobenzyl)-5'-N-methylcarboxamidoadenosine; 20125-40-0 / N-(1-methyl-2-phenylethyl)adenosine; 333DO1RDJY / Serotonin; 35920-39-9 / Adenosine-5'-(N-ethylcarboxamide); EC 2.7.11.12 / Cyclic GMP-Dependent Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; K72T3FS567 / Adenosine
  •  go-up   go-down


2. Carriero MV, Longanesi-Cattani I, Bifulco K, Maglio O, Lista L, Barbieri A, Votta G, Masucci MT, Arra C, Franco R, De Rosa M, Stoppelli MP, Pavone V: Structure-based design of an urokinase-type plasminogen activator receptor-derived peptide inhibiting cell migration and lung metastasis. Mol Cancer Ther; 2009 Sep;8(9):2708-17
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structure-based design of an urokinase-type plasminogen activator receptor-derived peptide inhibiting cell migration and lung metastasis.
  • The urokinase-type plasminogen activator receptor (uPAR) plays a central role in sustaining the malignant phenotype and promoting tumor metastasis.
  • Here, we describe the generation of new peptide inhibitors of cell migration and invasion derived from SRSRY by a drug design approach.
  • Ac-Arg-Glu-Arg-Phe-NH(2) (i.e., RERF), which adopts a turned structure in solution, was selected for its ability to potently prevent SRSRY-directed cell migration.
  • Fluorescein-RERF associates with very high affinity to RBL-2H3 rat basophilic leukemia cells expressing the human formyl peptide receptor (FPR).
  • Accordingly, femtomolar concentrations of RERF prevent agonist-dependent internalization of FPR and inhibit N-formyl-Met-Leu-Phe-dependent migration in a dose-dependent manner.
  • In the absence of FPR, fluorescein-RERF binds to cell surface at picomolar concentrations in an alphav integrin-dependent manner.
  • The involvement of vitronectin receptor is further supported by the findings that 100 pmol/L RERF selectively inhibits vitronectin-dependent RBL-2H3 cell migration and prevents SRSRY-triggered uPAR/alphav association.
  • Furthermore, RERF reduces the speed of wound closure and the extent of Matrigel invasion by human fibrosarcoma HT1080 cells without affecting cell proliferation.
  • Finally, a 3- to 5-fold reduction of lung metastasis number and size in nude mice following i.v. injection of green fluorescent protein-expressing HT1080 cells in the presence of 3.32 mg/kg RERF is observed.
  • Our findings indicate that RERF effectively prevents malignant cell invasion in vivo with no signs of toxicity and may represent a promising prototype drug for anticancer therapy.
  • [MeSH-major] Cell Movement / drug effects. Lung Neoplasms / secondary. Neoplasm Metastasis / prevention & control. Peptide Fragments / pharmacology. Receptors, Urokinase Plasminogen Activator / chemistry
  • [MeSH-minor] Animals. Female. Fibrosarcoma / pathology. Humans. Immunoprecipitation. Mice. Mice, Nude. Microscopy, Fluorescence. Models, Molecular. Nuclear Magnetic Resonance, Biomolecular. Protein Conformation. Rats

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19706734.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptide Fragments; 0 / Receptors, Urokinase Plasminogen Activator
  •  go-up   go-down


3. Ligresti A, Cascio MG, Pryce G, Kulasegram S, Beletskaya I, De Petrocellis L, Saha B, Mahadevan A, Visintin C, Wiley JL, Baker D, Martin BR, Razdan RK, Di Marzo V: New potent and selective inhibitors of anandamide reuptake with antispastic activity in a mouse model of multiple sclerosis. Br J Pharmacol; 2006 Jan;147(1):83-91
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New potent and selective inhibitors of anandamide reuptake with antispastic activity in a mouse model of multiple sclerosis.
  • We have now re-examined the activity of O-2093 in vivo and synthesized four structural analogs (O-2247, O-2248, O-3246, and O-3262), whose activity was assessed in: (a) binding assays carried out with membranes from cells overexpressing the human CB(1) and CB(2) receptors;.
  • (b) assays of transient receptor potential of the vanilloid type-1 (TRPV1) channel functional activity (measurement of [Ca(2+)](i));.
  • (c) [(14)C]AEA cellular uptake and hydrolysis assays in rat basophilic leukaemia (RBL-2H3) cells;.
  • Like O-2093, the other four compounds exhibited low affinity in CB(1) (K(i) from 1.3 to >10 microM) and CB(2) binding assays (1.3<K(i)< 8 microM), low potency and efficacy in a TRPV1 functional assay (EC(50)>10 microM), very low potency as fatty acid amide hydrolase (FAAH) inhibitors (IC(50)>25 microM) and were inactive in the 'tetrad' up to a 30 mg kg(-1) dose (i.v.).
  • These data confirm the potential utility of selective AEA uptake inhibitors as anti-spasticity drugs in MS and, given the very subtle chemical differences between potent and weak inhibitors of uptake, support further the existence of a specific mechanism for this process.
  • [MeSH-major] Arachidonic Acids / antagonists & inhibitors. Multiple Sclerosis / drug therapy. Muscle Spasticity / drug therapy. Neuromuscular Blocking Agents / pharmacology. Polyunsaturated Alkamides / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line. Disease Models, Animal. Endocannabinoids. Mice. Rats

  • MedlinePlus Health Information. consumer health - Multiple Sclerosis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Mar 2;404(6773):84-7 [10716447.001]
  • [Cites] Eur J Pharmacol. 2003 Jun 27;471(3):185-93 [12826237.001]
  • [Cites] Pharmacol Ther. 2004 Nov;104(2):117-35 [15518883.001]
  • [Cites] Eur J Pharmacol. 2004 Jan 26;484(2-3):249-57 [14744610.001]
  • [Cites] Prostaglandins Other Lipid Mediat. 2002 Aug;68-69:619-31 [12432948.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Feb 23;281(2):444-51 [11181068.001]
  • [Cites] Biochem Pharmacol. 2003 May 1;65(9):1473-81 [12732359.001]
  • [Cites] FEBS Lett. 2000 Oct 13;483(1):52-6 [11033355.001]
  • [Cites] Neuropharmacology. 2004;47 Suppl 1:345-58 [15464149.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5802-7 [10318965.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Aug 19;262(1):275-84 [10448105.001]
  • [Cites] FASEB J. 2001 Feb;15(2):300-2 [11156943.001]
  • [Cites] Eur J Biochem. 2001 Apr;268(7):1982-9 [11277920.001]
  • [Cites] Bioorg Med Chem. 2004 Oct 1;12(19):5161-9 [15351399.001]
  • [Cites] J Neurochem. 2005 Mar;92(6):1327-39 [15748152.001]
  • [Cites] Eur J Pharmacol. 2004 May 10;492(1):1-11 [15145699.001]
  • [Cites] Biochem Pharmacol. 1995 Jun 29;50(1):83-90 [7605349.001]
  • [Cites] Eur J Pharmacol. 2002 Mar 29;439(1-3):83-92 [11937096.001]
  • [Cites] J Biol Chem. 1997 Feb 7;272(6):3315-23 [9013571.001]
  • [Cites] Br J Pharmacol. 2000 Jan;129(2):227-30 [10694225.001]
  • [Cites] FASEB J. 2005 Aug;19(10):1338-40 [15941768.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Oct 4;215(1):89-97 [7575630.001]
  • [Cites] Biochemistry. 2004 Jun 29;43(25):8184-90 [15209515.001]
  • [Cites] Nat Rev Drug Discov. 2004 Sep;3(9):771-84 [15340387.001]
  • [Cites] J Org Chem. 1996 May 31;61(11):3849-3862 [11667239.001]
  • [Cites] Nature. 1994 Dec 15;372(6507):686-91 [7990962.001]
  • [Cites] Eur Neuropsychopharmacol. 2006 Jan;16(1):7-18 [16006105.001]
  • [Cites] Biochem J. 2004 May 15;380(Pt 1):265-72 [14969584.001]
  • [Cites] J Pharmacol Exp Ther. 2002 Mar;300(3):984-91 [11861807.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 8;101(23):8756-61 [15138300.001]
  • [Cites] Cell Mol Life Sci. 2005 Feb;62(3):386-95 [15723173.001]
  • [Cites] Pharmacol Biochem Behav. 1991 Nov;40(3):471-8 [1666911.001]
  • [Cites] Br J Pharmacol. 2003 Nov;140(5):802-8 [12970089.001]
  • [Cites] Science. 1992 Dec 18;258(5090):1946-9 [1470919.001]
  • [Cites] Nature. 1996 Nov 7;384(6604):83-7 [8900284.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):4269-74 [12655057.001]
  • [Cites] Pain. 2000 Nov;88(2):205-15 [11050376.001]
  • [Cites] J Med Chem. 2003 Apr 10;46(8):1512-22 [12672252.001]
  • (PMID = 16284631.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA008904; United States / NIDA NIH HHS / DA / DA-09789; United Kingdom / Multiple Sclerosis Society / / 835; United Kingdom / Multiple Sclerosis Society / / 541; United States / NIDA NIH HHS / DA / P01 DA009789; United States / NIDA NIH HHS / DA / DA-08904
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arachidonic Acids; 0 / Endocannabinoids; 0 / Neuromuscular Blocking Agents; 0 / Polyunsaturated Alkamides; UR5G69TJKH / anandamide
  • [Other-IDs] NLM/ PMC1615845
  •  go-up   go-down


Advertisement
4. Cui Y, Hou X, Chen J, Xie L, Yang L, Le Y: Sesamin inhibits bacterial formylpeptide-induced inflammatory responses in a murine air-pouch model and in THP-1 human monocytes. J Nutr; 2010 Feb;140(2):377-81
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sesamin inhibits bacterial formylpeptide-induced inflammatory responses in a murine air-pouch model and in THP-1 human monocytes.
  • The reaction of human leukocytes to chemoattractants is an important component of the host immune response and also plays a crucial role in the development of inflammation.
  • In this study, we examined the effect of sesamin on inflammatory responses elicited by the bacterial chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fMLF) in vitro and in vivo and explored the mechanisms involved. fMLF is recognized by a human G protein-coupled receptor formyl peptide receptor (FPR) on phagocytic leukocytes.
  • Sesamin at concentrations between 12.5 and 50 micromol/L inhibited fMLF-induced chemotaxis of human monocyte cell line THP-1 differentiated with dibutyryl cyclic AMP (P < 0.01).
  • Similarly, sesamin inhibited FPR-transfected rat basophilic leukemia cell [epitope-tagged human FPR (ETFR) cell] migration toward fMLF (P < 0.01).
  • In fMLF-induced inflammation in a murine air-pouch model, intraperitoneal administration of sesamin (12 mgkg(-1)d(-1) for 2 d) suppressed leukocyte infiltration into the air pouch induced by fMLF [(62.89 +/- 7.93) x 10(4) vs. (19.67 +/- 4.43) x 10(4) cells/air pouch; n = 9; P < 0.001].
  • Ca(2+) mobilization and mitogen-activated protein kinase extracellular signal-regulated kinase (ERK1/2) activation are involved in fMLF-induced leukocyte migration.
  • Pretreatment of ETFR cells with sesamin inhibited fMLF-induced ERK1/2 phosphorylation in a dose-dependent manner but did not affect fMLF-induced Ca(2+) flux.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Chemotaxis, Leukocyte / drug effects. Dioxoles / pharmacology. Leukemic Infiltration / drug therapy. Lignans / pharmacology. Monocytes / drug effects. Plant Extracts / pharmacology. Sesamum / chemistry
  • [MeSH-minor] Animals. Bacteria / metabolism. Basophils / drug effects. Bucladesine. Calcium / metabolism. Cell Line. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Inflammation / chemically induced. Inflammation / drug therapy. Inflammation / metabolism. Leukemia / drug therapy. Mice. Mice, Inbred C57BL. Mitogen-Activated Protein Kinase 1 / metabolism. Models, Animal. N-Formylmethionine Leucyl-Phenylalanine. NF-kappa B / antagonists & inhibitors. Phosphorylation. Phytotherapy. Rats. Receptors, Formyl Peptide / metabolism. Signal Transduction / drug effects

  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20032476.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Dioxoles; 0 / Lignans; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Receptors, Formyl Peptide; 59880-97-6 / N-Formylmethionine Leucyl-Phenylalanine; 63X7MBT2LQ / Bucladesine; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; S7946O4P76 / sesamin; SY7Q814VUP / Calcium
  •  go-up   go-down


5. Sakai S, Sugawara T, Kishi T, Yanagimoto K, Hirata T: Effect of glucosamine and related compounds on the degranulation of mast cells and ear swelling induced by dinitrofluorobenzene in mice. Life Sci; 2010 Feb 27;86(9-10):337-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MAIN METHODS: Dinitrophenyl (DNP)-IgE-sensitized rat basophilic leukemia RBL-2H3 cells were treated with glucosamine-HCl (GlcN-HCl), N-acetylglucosamine (GlcNAc), chitin oligomer or chitosan oligomer.
  • One hour after the final administration, mice were challenged by DNFB to induce ear swelling.
  • KEY FINDINGS: GlcN-HCl significantly inhibited the antigen-induced degranulation of RBL-2H3 cells at higher than 0.01 mg/mL for 24h-treatment while GlcNAc, a chitin oligomer and a chitosan oligomer had no effect.
  • GlcN-HCl and GlcNAc significantly suppressed the antigen-induced up-regulation of TNF-alpha and IL-6 mRNA.
  • [MeSH-major] Cell Degranulation / physiology. Dinitrofluorobenzene / toxicity. Ear. Edema / drug therapy. Glucosamine / therapeutic use. Mast Cells / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cells, Cultured. Female. Mice. Mice, Inbred BALB C. Rats

  • MedlinePlus Health Information. consumer health - Edema.
  • Hazardous Substances Data Bank. GLUCOSAMINE .
  • Hazardous Substances Data Bank. 1-FLUORO-2,4-DINITROBENZENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20093129.001).
  • [ISSN] 1879-0631
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] D241E059U6 / Dinitrofluorobenzene; N08U5BOQ1K / Glucosamine
  •  go-up   go-down


6. Qu X, Li Y, Liu J, Xu L, Zhang Y, Hu X, Hou K, Liu Y: Cbl-b promotes chemotherapy-induced apoptosis in rat basophilic leukemia cells by suppressing PI3K/Akt activation and enhancing MEK/ERK activation. Mol Cell Biochem; 2010 Jul;340(1-2):107-14
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cbl-b promotes chemotherapy-induced apoptosis in rat basophilic leukemia cells by suppressing PI3K/Akt activation and enhancing MEK/ERK activation.
  • The ubiquitin ligase Cbl-b is a negative regulator of the PI3K/Akt pathway, the survival pathway implicated in chemotherapy resistance.
  • The PI3K inhibitor LY294002, not the ERK inhibitor PD98059, enhanced the apoptosis.
  • Over expression of Cbl-b significantly enhanced VP-16-induced cell apoptosis with inhibition of Akt activity, while a dominant negative (DN) RING Finger domain mutation completely abolished this enhancement.
  • On the other hand, ERK activity was enhanced by Cbl-b, and the ERK inhibitor PD98059 reversed Cbl-b-enhanced apoptosis.
  • The consistent results were also showed in the process of Ara-c treatment.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Leukemia, Basophilic, Acute / enzymology. Mitogen-Activated Protein Kinase Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-cbl / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival. Cytarabine / pharmacology. Dose-Response Relationship, Drug. Enzyme Activation. Enzyme Inhibitors / pharmacology. Etoposide / pharmacology. Inhibitory Concentration 50. Mutation. Rats. Time Factors. Transfection

  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • 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. 2006 Nov 1;177(9):5980-9 [17056522.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1779-86 [14604964.001]
  • [Cites] Nature. 2000 Jan 13;403(6766):211-6 [10646608.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1921-30 [17581609.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1203-11 [17283156.001]
  • [Cites] Oncogene. 1995 Jun 15;10(12):2367-77 [7784085.001]
  • [Cites] J Biol Chem. 2001 Feb 16;276(7):4872-8 [11087752.001]
  • [Cites] J Immunol. 2008 Oct 15;181(8):5331-9 [18832689.001]
  • [Cites] Cancer. 2003 Oct 1;98(7):1521-30 [14508841.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1022-4 [17475912.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Feb 29;367 (1):183-9 [18164258.001]
  • [Cites] Cancer Res. 2008 Aug 1;68(15):6271-80 [18676851.001]
  • [Cites] Eur J Haematol. 2003 Apr;70(4):219-24 [12656744.001]
  • [Cites] FEBS Lett. 2009 Jul 7;583(13):2255-62 [19508871.001]
  • [Cites] J Pathol. 2009 Jun;218(2):248-55 [19274672.001]
  • [Cites] J Biol Chem. 2005 Sep 9;280(36):31498-507 [16014620.001]
  • [Cites] Br J Haematol. 2005 Jun;129(5):677-86 [15916691.001]
  • [Cites] Biochim Biophys Acta. 2006 Sep;1763(9):958-68 [16905201.001]
  • [Cites] Oncogene. 2002 Feb 21;21(9):1423-33 [11857085.001]
  • [Cites] Mol Cancer Ther. 2008 Oct;7(10 ):3141-9 [18852117.001]
  • [Cites] Nat Immunol. 2001 Sep;2(9):870-5 [11526404.001]
  • [Cites] Immunity. 2007 May;26(5):567-78 [17493844.001]
  • [Cites] Nature. 2000 Jan 13;403(6766):216-20 [10646609.001]
  • [Cites] Mutagenesis. 2006 Mar;21(2):105-14 [16500949.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Aug 24;213(3):837-44 [7654245.001]
  • [Cites] Neoplasia. 2008 Oct;10 (10 ):1083-91 [18813358.001]
  • (PMID = 20177738.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; EC 2.3.2.27 / Proto-Oncogene Proteins c-cbl; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 6.3.2.19 / Cblb protein, rat
  •  go-up   go-down


7. Cho YS, Kim CH, Surh JH, Kang NS, Yoo SE, Cheon HG: Identification of 4-[4-(4-fluoro-phenyl)-thiazol-2-ylamino]-2,6-dimethyl-phenol (KR-33749) as an inhibitor of 5-lipoxygenase with potent antiinflammatory activity. Pharmacology; 2010;86(2):65-72
Hazardous Substances Data Bank. 1-CHLORO-2,4-DINITROBENZENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of 4-[4-(4-fluoro-phenyl)-thiazol-2-ylamino]-2,6-dimethyl-phenol (KR-33749) as an inhibitor of 5-lipoxygenase with potent antiinflammatory activity.
  • BACKGROUND/AIM: To discover new 5-lipoxygenase (5-LO) inhibitors applicable to inflammation-related skin disease, we identified and examined antiinflammatory properties of a novel 5-LO inhibitor, KR-33749, in vitro and in vivo.
  • METHODS: 5-LO enzyme activity was assayed using insect cell lysates overexpressing rat 5-LO.
  • The leukotriene B(4) (LTB(4)) level was assayed in rat basophilic leukemia (RBL-1) cell line.
  • RESULTS: KR-33749 inhibited 5-LO activity with an IC(50) value of 70.5 +/- 6.0 nmol/l in parallel with LTB(4) inhibition in RBL-1 cells.
  • CONCLUSION: Our results show that KR-33749, a new 5-LO inhibitor exhibits potent antiinflammatory activities in vitro as well as in vivo.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Arachidonate 5-Lipoxygenase / metabolism. Lipoxygenase Inhibitors / pharmacology. Lipoxygenase Inhibitors / therapeutic use. Thiazoles / pharmacology. Thiazoles / therapeutic use. Xylenes / pharmacology. Xylenes / therapeutic use
  • [MeSH-minor] Animals. Arachidonic Acid / toxicity. Cell Line, Tumor. Dermatitis, Atopic / drug therapy. Dermatitis, Atopic / immunology. Dermatitis, Atopic / pathology. Dinitrochlorobenzene / toxicity. Dose-Response Relationship, Drug. Edema / prevention & control. Isoenzymes / antagonists & inhibitors. Leukotriene B4 / metabolism. Leukotriene B4 / secretion. Male. Mice. Mice, Inbred BALB C. Osmolar Concentration. Rats. Recombinant Proteins / antagonists & inhibitors. Skin / drug effects. Skin / pathology. Skin Diseases / drug therapy. Time Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20639685.001).
  • [ISSN] 1423-0313
  • [Journal-full-title] Pharmacology
  • [ISO-abbreviation] Pharmacology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / 4-(4-(4-fluorophenyl)thiazol-2-ylamino)-2,6-dimethylphenol; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Isoenzymes; 0 / Lipoxygenase Inhibitors; 0 / Recombinant Proteins; 0 / Thiazoles; 0 / Xylenes; 1HGW4DR56D / Leukotriene B4; 27YG812J1I / Arachidonic Acid; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; GE3IBT7BMN / Dinitrochlorobenzene
  •  go-up   go-down


8. Kaur S, Sur R, Liebel FT, Southall MD: Induction of prostaglandin D2 through the p38 MAPK pathway is responsible for the antipruritic activity of sertaconazole nitrate. J Invest Dermatol; 2010 Oct;130(10):2448-56
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of prostaglandin D2 through the p38 MAPK pathway is responsible for the antipruritic activity of sertaconazole nitrate.
  • Prostaglandin D(2) (PGD(2)) is known to have antipruritic activity by suppressing histamine release.
  • However, agents that can topically induce PGD(2) for itch relief are not well established.
  • The antimycotic sertaconazole nitrate (STZ) has been shown to exhibit anti-itch properties; however, the mechanism for this activity has not been elucidated.
  • STZ mitigated degranulation of RBL-2H3 (rat basophilic leukemia) mast cells induced by compound 48/80, a pruritogenic agent known to promote the release of histamine, and augmented PGD(2) production in mast cells and macrophages.
  • Addition of exogenous PGD(2) abrogated compound 48/80-induced degranulation by acting through the prostanoid D receptor 1 (DP1).
  • STZ induced p38 mitogen-activated protein kinase (MAPK) phosphorylation in mast cells and a pharmacological inhibitor of p38 MAPK, SB203580, resulted in the attenuation of PGD(2) levels.
  • [MeSH-major] Imidazoles / pharmacology. Macrophages / drug effects. Mast Cells / drug effects. Prostaglandin D2 / metabolism. Pruritus / drug therapy. Thiophenes / pharmacology. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Administration, Topical. Animals. Antifungal Agents / pharmacology. Cell Degranulation / drug effects. Cell Line. Drug Interactions. Histamine / metabolism. Indoles / pharmacology. Mice. Mice, Inbred ICR. Rats. Receptors, Prostaglandin / metabolism. p-Methoxy-N-methylphenethylamine / pharmacology

  • MedlinePlus Health Information. consumer health - Itching.
  • Hazardous Substances Data Bank. HISTAMINE .
  • 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 = 20505747.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Imidazoles; 0 / Indoles; 0 / MK-0524; 0 / Receptors, Prostaglandin; 0 / Thiophenes; 0 / prostanoid D receptor 1, mouse; 4091-50-3 / p-Methoxy-N-methylphenethylamine; 72W71I16EG / sertaconazole; 820484N8I3 / Histamine; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; RXY07S6CZ2 / Prostaglandin D2
  •  go-up   go-down


9. Kobayashi S, Tanabe S: Evaluation of the anti-allergic activity of Citrus unshiu using rat basophilic leukemia RBL-2H3 cells as well as basophils of patients with seasonal allergic rhinitis to pollen. Int J Mol Med; 2006 Mar;17(3):511-5
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of the anti-allergic activity of Citrus unshiu using rat basophilic leukemia RBL-2H3 cells as well as basophils of patients with seasonal allergic rhinitis to pollen.
  • The anti-allergic activity of the 50% methanol extract of Citrus unshiu powder (MEC) was examined.
  • Fifty percent methanol extract of MEC powder showed potent inhibitory activity against histamine release from basophils of patients suffering from seasonal allergic rhinitis to ceder pollen.
  • To examine this anti-allergic mechanism in detail, we next used rat basophlilic leukemia RBL-2H3 cells.
  • Since MEC contains a variety of flavonoids, we selected nobiletin, hesperetin, and hesperidin (hesperetin glycoside) as representative compounds, and further evaluated these inhibitory activities.
  • Among the flavonoids tested, hesperetin was the most potent, while hesperidin had far less, if any, inhibitory activity.
  • [MeSH-major] Anti-Allergic Agents / therapeutic use. Basophils / drug effects. Citrus. Leukemia, Basophilic, Acute / immunology. Phytotherapy. Pollen / immunology. Rhinitis, Allergic, Seasonal / drug therapy
  • [MeSH-minor] Animals. Cell Degranulation / drug effects. Flavonoids / chemistry. Flavonoids / pharmacology. Flavonoids / therapeutic use. Histamine Release / drug effects. Humans. Immunoglobulin E / metabolism. Phosphatidylinositol 3-Kinases. Phosphorylation / drug effects. Plant Preparations / pharmacology. Plant Preparations / therapeutic use. Proto-Oncogene Proteins c-akt / metabolism. Rats. beta-N-Acetylhexosaminidases / secretion

  • Genetic Alliance. consumer health - Allergic rhinitis.
  • MedlinePlus Health Information. consumer health - Hay Fever.
  • MedlinePlus Health Information. consumer health - Herbal Medicine.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16465400.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anti-Allergic Agents; 0 / Flavonoids; 0 / Plant Preparations; 37341-29-0 / Immunoglobulin E; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.2.1.52 / beta-N-Acetylhexosaminidases
  •  go-up   go-down


10. Yokohama A, Tsukamoto N, Hatsumi N, Suto M, Akiba T, Uchiumi H, Maehara T, Matsushima T, Karasawa M, Murakami H, Shinonome S, Saito H, Nojima Y: Acute basophilic leukemia lacking basophil-specific antigens: the importance of cytokine receptor expression in differential diagnosis. Int J Hematol; 2002 Apr;75(3):309-13
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute basophilic leukemia lacking basophil-specific antigens: the importance of cytokine receptor expression in differential diagnosis.
  • De novo acute basophilic leukemia (ABL) is a rare form of myeloid leukemia.
  • The low prevalence of ABL makes it difficult to define its clinical characteristics and to establish an effective therapeutic protocol.
  • We present here a case of de novo ABL in a 64-year-old Japanese man.
  • (1) metachromasia with toluidine blue stain, (2) intracytoplasmic theta granules identified by electron microscopy, and (3) findings obtained from extensive immunophenotypic analysis.
  • Although blast cells lacked basophil-specific antigens such as CDw17, CD88, and FcepsilonRI, an expression profile of cytokine receptors including CD116 (GM-CSF receptor), CD117 (c-kit), and CD123 (IL-3 receptor alpha) helped to define the cellular lineage in our case.
  • The patient achieved complete remission with intensive chemotherapy composed of idarubicin and cytosine arabinoside and was disease free during the following 30 months.
  • [MeSH-major] Antigens, CD / blood. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Basophilic, Acute / diagnosis. Mast Cells / immunology. Receptors, Cytokine / genetics
  • [MeSH-minor] Bone Marrow / pathology. Cytarabine / administration & dosage. Diagnosis, Differential. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Receptors, IgE / blood

  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pathology. 2000 Feb;32(1):52-5 [10740808.001]
  • [Cites] Exp Hematol. 1993 Jan;21(1):119-25 [7678084.001]
  • [Cites] J Allergy Clin Immunol. 1994 Dec;94(6 Pt 2):1177-83 [7798557.001]
  • [Cites] Br J Haematol. 1997 Jul;98(1):170-6 [9233581.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2288-92 [3258425.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):735-9 [7678463.001]
  • [Cites] Cytometry. 1999 Mar 1;35(3):249-59 [10082306.001]
  • [Cites] Blood. 1989 Aug 1;74(2):613-21 [2665851.001]
  • [Cites] Am J Hematol. 1989 Jul;31(3):173-80 [2787115.001]
  • [Cites] Blood. 1990 Nov 15;76(10):1956-61 [1700728.001]
  • [Cites] Cancer Genet Cytogenet. 1995 Oct 15;84(2):99-104 [8536230.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2333-42 [10498605.001]
  • [Cites] Eur J Clin Invest. 1995 Oct;25(10):715-20 [8557056.001]
  • [Cites] Blood. 1989 May 1;73(6):1504-12 [2653458.001]
  • [Cites] Blood. 1989 Aug 1;74(2):565-71 [2546627.001]
  • [Cites] Blood. 1999 May 15;93(10):3338-46 [10233886.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Blood. 1992 Dec 15;80(12):3009-21 [1281684.001]
  • [Cites] Neoplasma. 1998;45(4):198-203 [9890661.001]
  • [Cites] Blood. 1982 Jul;60(1):38-45 [7082845.001]
  • [Cites] Immunology. 1996 Apr;87(4):535-43 [8675206.001]
  • [Cites] Br J Haematol. 1995 Mar;89(3):650-2 [7734371.001]
  • [Cites] Leuk Lymphoma. 1999 Jan;32(3-4):269-78 [10037024.001]
  • [Cites] Leuk Lymphoma. 1995;18 Suppl 1:57-60 [7496356.001]
  • [Cites] Blood. 1992 Nov 1;80(9):2237-45 [1384799.001]
  • [Cites] Am J Clin Pathol. 1991 Aug;96(2):160-70 [1862771.001]
  • [Cites] Adv Immunol. 1992;52:333-423 [1332448.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1987 Spring;9(1):27-32 [2438957.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2343-56 [10498606.001]
  • [Cites] Cancer. 1995 Jan 1;75(1):110-4 [7804964.001]
  • [Cites] J Allergy Clin Immunol. 2000 Dec;106(6):1190-5 [11112905.001]
  • [Cites] J Med. 1995;26(5-6):235-40 [8721900.001]
  • [Cites] J Allergy Clin Immunol. 2000 Aug;106(2):321-8 [10932077.001]
  • (PMID = 11999362.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Receptors, Cytokine; 0 / Receptors, IgE; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
  •  go-up   go-down


11. Li Y, Lee SH, Le QT, Kim MM, Kim SK: Anti-allergic effects of phlorotannins on histamine release via binding inhibition between IgE and Fc epsilonRI. J Agric Food Chem; 2008 Dec 24;56(24):12073-80
MedlinePlus Health Information. consumer health - Allergy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, anti-allergic activities of phloroglucinol derivatives were assessed on human basophilic leukemia (KU812) and rat basophilic leukemia (RBL-2H3) cell lines using a histamine release assay.
  • Both compounds 1 and 3 exhibited a significant inhibitory activity against histamine release.
  • Meanwhile, the potential inhibitory mechanism was also suggested as the suppression of binding activity between IgE and Fc epsilonRI by the cytometric analysis.
  • These results suggested that compounds 1 and 3 could be the key effectors in the crude methanol extract of EC against allergy disease and used as novel candidates for development in the cosmetic and drug industries potentially.
  • [MeSH-major] Anti-Allergic Agents / pharmacology. Histamine Release / drug effects. Hypersensitivity / drug therapy. Immunoglobulin E / immunology. Phaeophyta / chemistry. Phloroglucinol / pharmacology. Plant Extracts / pharmacology. Receptors, IgE / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Protein Binding / drug effects. Rats

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19053379.001).
  • [ISSN] 1520-5118
  • [Journal-full-title] Journal of agricultural and food chemistry
  • [ISO-abbreviation] J. Agric. Food Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Allergic Agents; 0 / Plant Extracts; 0 / Receptors, IgE; 37341-29-0 / Immunoglobulin E; DHD7FFG6YS / Phloroglucinol
  •  go-up   go-down


12. Zhu J, Wang O, Ruan L, Hou X, Cui Y, Wang JM, Le Y: The green tea polyphenol (-)-epigallocatechin-3-gallate inhibits leukocyte activation by bacterial formylpeptide through the receptor FPR. Int Immunopharmacol; 2009 Aug;9(9):1126-30
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We examined the capacity of epigallocatechin gallate (EGCG) to regulate leukocyte responses to bacterial chemotactic peptide N-formylmethionyl-leucyl-phenylalanine (fMLF), which is recognized by a human G protein-coupled receptor FPR on phagocytic leukocytes.
  • Pretreatment of human monocytic cells or FPR-transfected rat basophilic leukemia cells (ETFR cells) with EGCG significantly inhibited fMLF-induced chemotaxis.
  • Mechanistic studies revealed that EGCG dose-dependently suppressed fMLF-induced calcium flux in monocytic cells and ETFR cells. fMLF-induced ETFR cell migration was significantly inhibited by a specific MEK1/2 inhibitor, PD98059, which was associated with reduction in fMLF-induced ERK1/2 phosphorylation.
  • [MeSH-minor] Animals. Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors. Camellia sinensis / immunology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / immunology. Flavonoids / pharmacology. Humans. Inflammation. Injections, Intraperitoneal. Leukemia, Basophilic, Acute / blood. Leukemia, Basophilic, Acute / drug therapy. Leukemia, Basophilic, Acute / immunology. Mice. Rats. Receptors, Formyl Peptide / genetics. Receptors, Formyl Peptide / immunology. Receptors, Formyl Peptide / metabolism. Signal Transduction / drug effects. Signal Transduction / immunology. Transfection. Transgenes

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 19426837.001).
  • [ISSN] 1878-1705
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antioxidants; 0 / Flavonoids; 0 / Receptors, Formyl Peptide; 59880-97-6 / N-Formylmethionine Leucyl-Phenylalanine; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
  •  go-up   go-down


13. Knipping K, van Esch EC, Wijering SC, van der Heide S, Dubois AE, Garssen J: In vitro and in vivo anti-allergic effects of Arctium lappa L. Exp Biol Med (Maywood); 2008 Nov;233(11):1469-77

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The discovery of drugs that can be used for the treatment of allergic disease is important in human health.
  • AL was selected out of 10,000 herbal extracts in a set-up for high throughput screening in which the degree of degranulation was monitored by the release of beta-hexosaminidase from rat basophil leukemia (RBL-2H3) cells.
  • The AL extract significantly reduced degranulation and biosynthesis of cys-leukotrienes of human basophils in peripheral blood mono-nuclear cells (PBMCs) (50% inhibitory concentration [IC(50)] = 8.3 and 11.4 microg/ml, respectively).
  • Viability and metabolic activity of the PBMCs were not affected.
  • Although arctiin, the active component of AL that has been described in the literature, was not able to reduce degranulation in RBL-2H3 cells, a single high-performance liquid chromatography (HPLC) fraction from the AL extract inhibited beta-hexosaminidase release (IC(50) = 22.2 microg/ml).
  • In addition, this active component was able to inhibit acute skin response in mice in vivo, indicating that AL is a very promising natural component for use in anti-allergic treatment.
  • [MeSH-minor] Animals. Basophil Degranulation Test. Basophils / drug effects. Basophils / metabolism. Chemical Fractionation. Chromatography, High Pressure Liquid. Ear Diseases / chemically induced. Ear Diseases / drug therapy. Edema / chemically induced. Edema / drug therapy. Humans. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / metabolism. Leukotrienes / biosynthesis. Mice. Rats

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18703753.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Allergic Agents; 0 / Anti-Inflammatory Agents; 0 / Leukotrienes; 0 / Plant Extracts
  •  go-up   go-down


14. Abe M, Shibata K, Urata H, Sakata N, Katsuragi T: Induction of leukotriene C4 synthase after the differentiation of rat basophilic leukemia cells with retinoic acid and a low dose of actinomycin D and its suppression with methylprednisolone. J Cell Physiol; 2003 Jul;196(1):154-64
Hazardous Substances Data Bank. METHYLPREDNISOLONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of leukotriene C4 synthase after the differentiation of rat basophilic leukemia cells with retinoic acid and a low dose of actinomycin D and its suppression with methylprednisolone.
  • LTC(4) S activity in rat basophilic leukemia-1 (RBL-1) cells increased after culture in the presence of retinoic acid (RA) analogues, which was inhibited by cycloheximide or actinomycin D (ACD).
  • Unexpectedly, the co-addition of a low dose of ACD with RA further potentiated the upregulation of the LTC(4) S activity.
  • When stimulated with calcium ionophore A23187, control cells did not produce cysLTs, but RA-treated cells generated cysLTs and the co-addition of ACD further increased.
  • While LTC(4) S mRNA and protein increased in the cells treated with RA, the co-addition of ACD further potentiated both in proportion to the LTC(4) S activity.
  • The effect of ACD was considered to enhance the transcription rate of LTC(4) S gene, but not the mRNA-stability.
  • The addition of methylprednisolone (MP) inhibited generation of cysLTs from the cells with A23187-stimulation and also did LTC(4) S activity, but did not inhibit 5-lipoxygenase (5-LOX).
  • The suppression of LTC(4) S with MP showed a dependent manner on the time-point and duration of MP-treatment after RA-addition which was correlated with reduction in LTC(4) S mRNA and protein.
  • The cells cultured with RA plus ACD contained more histamine, chymase activity, and granules in the cytoplasm than the control cells, suggesting differentiation to mature mast cells.
  • In consideration of RA-differentiation therapy, it may be of pathophysiological relevance that the antineoplastic agents potentiate RA-induced, steroid-sensitive, induction of LTC(4) S in RBL-1 cells.
  • [MeSH-major] Cell Differentiation / drug effects. Dactinomycin / antagonists & inhibitors. Dactinomycin / pharmacology. Glutathione Transferase / biosynthesis. Leukemia, Basophilic, Acute / enzymology. Methylprednisolone / pharmacology. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Calcimycin / pharmacology. Cell Line. Cell Size / drug effects. Chymases. Cycloheximide / pharmacology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Histamine / metabolism. Interleukin-4 / genetics. Lipoxygenase / metabolism. RNA Stability / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Serine Endopeptidases / metabolism. Solubility. Time Factors. Transcription, Genetic / drug effects

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. DACTINOMYCIN .
  • Hazardous Substances Data Bank. HISTAMINE .
  • Hazardous Substances Data Bank. CYCLOHEXIMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12767051.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 1CC1JFE158 / Dactinomycin; 207137-56-2 / Interleukin-4; 37H9VM9WZL / Calcimycin; 5688UTC01R / Tretinoin; 820484N8I3 / Histamine; 98600C0908 / Cycloheximide; EC 1.13.11.12 / Lipoxygenase; EC 2.5.1.18 / Glutathione Transferase; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.39 / Chymases; EC 4.4.1.20 / leukotriene-C4 synthase; X4W7ZR7023 / Methylprednisolone
  •  go-up   go-down


15. Scolyer RA, Brun M, D'Rozario J, Webb M: Acute basophilic leukemia presenting with abnormal liver function tests and the absence of blast cells in the peripheral blood. Pathology; 2000 Feb;32(1):52-5
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute basophilic leukemia presenting with abnormal liver function tests and the absence of blast cells in the peripheral blood.
  • Acute basophilic leukemia is an uncommon form of acute leukemia, rarely occurring as a de novo disease.
  • We describe a case of de novo acute basophilic leukemia occurring in a 47-year-old man who presented with abnormal liver function tests in the absence of leukemic infiltration of the liver.
  • We postulate that this presentation occurred as a consequence of pathophysiological features of the malignant basophilic blast cells.
  • [MeSH-major] Leukemia, Basophilic, Acute / diagnosis. Leukemic Infiltration / pathology. Liver / pathology. Liver Function Tests. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Cells / pathology. Cytarabine / therapeutic use. Cytoplasmic Granules / ultrastructure. Diagnosis, Differential. Drug Therapy, Combination. Fatal Outcome. Humans. Idarubicin / therapeutic use. Immunophenotyping. Karyotyping. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Liver Function Tests.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10740808.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
  •  go-up   go-down


16. Tries S, Neupert W, Laufer S: The mechanism of action of the new antiinflammatory compound ML3000: inhibition of 5-LOX and COX-1/2. Inflamm Res; 2002 Mar;51(3):135-43

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: We examined the effects of ML3000 and several non-steroidal antiinflammatory drugs (NSAIDs) on the synthesis of products of 5-LOX (LTB4, LTC4) and COX-1/2 (TXB2, PGE2) in vitro and ex vivo in order to further elucidate the mechanism of action of ML3000.
  • METHODS AND RESULTS: Using a human whole blood assay the effect of ML3000 on the shunt of arachidonic acid to the lipoxygenase pathway when COX is blocked was studied.
  • ML3000 (0.3, 1, 3, 10, 30 microg/ml) and indomethacin (0.3, 1, 3, 10, 30 microg/ml) concentration-dependently inhibited the synthesis of PGE2 (IC50 = 3.9 and 4.5 microM).
  • 5-lipoxygenase inhibition was further tested in a basophilic leukemia cell assay using RBL-1 cells.
  • ML3000 (1-10 microM) inhibited the synthesis of LTB4 in a concentration related manner (IC50: 3.6 microM).
  • In carrageenan induced rat paw edema, ML3000 and indomethacin completely blocked the formation of PGE2 in the inflamed tissue.
  • The LTB4 production in the inflamed paw was reduced to basal levels by ML3000 (10 +/- 1.4 pg/paw saline control and 7.5 +/- 1.3-5.9 +/- 3.2 pg/paw ML3000), whereas LTB4 levels remained markedly elevated as compared to saline control by indomethacin (30.7 pg/paw).
  • MK-886 and ML3000 at 10 mg/kg p.o. reduced LTB4 production to 29.8 +/- 4.9 and 30.1 +/- 2.8 pg/mg tissue as compared to control (54.2 +/- 7.4 mg/kg tissue).
  • LTB4 levels in the rat stomach were comparable to control (2.5 +/- 0.4 pg/mg protein) after oral administration of ML3000 (10, 30, 100 mg/kg), whereas oral treatment with indomethacin (0.3, 1, 3 mg/kg) or diclofenac (1, 3 mg/kg) increased LTB4 up to 9.2 +/- 2.3 or 8.9 +/- 1.6 pg/mg protein.
  • [MeSH-minor] Adult. Animals. Colon / drug effects. Colon / metabolism. Edema / drug therapy. Edema / metabolism. Humans. Leukotriene B4 / biosynthesis. Leukotriene C4 / biosynthesis. Male. Rats. Rats, Sprague-Dawley. Rats, Wistar. Stomach / drug effects. Stomach / metabolism. Thromboxane B2 / biosynthesis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12005204.001).
  • [ISSN] 1023-3830
  • [Journal-full-title] Inflammation research : official journal of the European Histamine Research Society ... [et al.]
  • [ISO-abbreviation] Inflamm. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Acetates; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 0 / Lipoxygenase Inhibitors; 0 / Pyrroles; 156897-06-2 / licofelone; 1HGW4DR56D / Leukotriene B4; 2CU6TT9V48 / Leukotriene C4; 54397-85-2 / Thromboxane B2
  •  go-up   go-down


17. Baumann MJ, Eggel A, Amstutz P, Stadler BM, Vogel M: DARPins against a functional IgE epitope. Immunol Lett; 2010 Oct 30;133(2):78-84
Hazardous Substances Data Bank. Omalizumab .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The monoclonal anti-IgE antibody omalizumab (Xolair is mostly used for the treatment of severe allergic asthma.
  • However, the requirement of high doses and suboptimal cost-effectiveness limits the use of the treatment.
  • Here we propose to use a new drug format based on non-immunoglobulin structures, potentially offering increased clinical efficacy while being more cost-effective.
  • For this purpose, DARPins™ (designed ankyrin repeat proteins) against the constant heavy chain region of IgE have been isolated.
  • Furthermore, anti-IgE DARPins were shown to inhibit proinflammatory mediator release from rat basophilic leukemia cells expressing human high-affinity IgE receptors with higher efficacy than the monoclonal anti-IgE antibody omalizumab.
  • DARPins may thus represent promising future drug candidates for the treatment of allergy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Asthma / drug therapy. Epitopes, B-Lymphocyte / immunology. Immunoglobulin E / metabolism. Recombinant Fusion Proteins / metabolism
  • [MeSH-minor] Animals. Ankyrin Repeat / genetics. Antibodies, Anti-Idiotypic. Antibodies, Monoclonal, Humanized. Antibody Affinity. Cell Line, Tumor. Humans. Immunoglobulin Constant Regions / genetics. Omalizumab. Protein Binding. Protein Engineering. Rats. Transgenes / genetics

  • MedlinePlus Health Information. consumer health - Asthma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20673836.001).
  • [ISSN] 1879-0542
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / DARPin E2 79; 0 / Epitopes, B-Lymphocyte; 0 / Immunoglobulin Constant Regions; 0 / Recombinant Fusion Proteins; 2P471X1Z11 / Omalizumab; 37341-29-0 / Immunoglobulin E
  •  go-up   go-down


18. Lahortiga I, Akin C, Cools J, Wilson TM, Mentens N, Arthur DC, Maric I, Noel P, Kocabas C, Marynen P, Lessin LS, Wlodarska I, Robyn J, Metcalfe DD: Activity of imatinib in systemic mastocytosis with chronic basophilic leukemia and a PRKG2-PDGFRB fusion. Haematologica; 2008 Jan;93(1):49-56
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of imatinib in systemic mastocytosis with chronic basophilic leukemia and a PRKG2-PDGFRB fusion.
  • BACKGROUND: Translocations involving region 5q31-32 (PDGFRB) have been reported in a variety of myeloproliferative diseases and are often associated with significant peripheral eosinophilia.
  • We report an unusual case of a patient presenting with peripheral basophilia and systemic mastocytosis in whom cytogenetic analysis revealed a t(4;5)(q21.1;q31.3).
  • DESIGN AND METHODS: We used molecular analyses to determine the role of PDGFRB in this case.
  • In agreement with this, the patient responded very well to imatinib with resolution of clinical symptoms, basophilia, and mast cell disease.
  • Molecular analyses revealed that PDGFRB, encoding an imatinib-sensitive tyrosine kinase, was fused to PRKG2.
  • Functional studies confirmed that the activity and transforming properties of PRKG2-PDGFRbeta were dependent on the disruption of the auto-inhibitory juxtamembrane domain.
  • CONCLUSIONS: Our results identify a second case of the PRKG2-PDGFRB fusion and confirm the unusual PDGFRB breakpoint associated with this fusion.
  • This work also illustrates the use of imatinib for the treatment of specific cases of systemic mastocytosis.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mastocytosis, Systemic / drug therapy. Mastocytosis, Systemic / genetics. Oncogene Proteins, Fusion / genetics. Piperazines / pharmacology. Pyrimidines / pharmacology. Receptor, Platelet-Derived Growth Factor beta / chemistry
  • [MeSH-minor] Animals. Benzamides. Bone Marrow / pathology. Cytogenetics. Humans. Imatinib Mesylate. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Mice. Middle Aged

  • Genetic Alliance. consumer health - Mast cell disease.
  • Genetic Alliance. consumer health - Systemic mastocytosis.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18166785.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  •  go-up   go-down


19. Li L, Ji H, Sheng L, Zhang Y, Lai Y, Chen X: The anti-inflammatory effects of ZLJ-6, a novel dual cyclooxygenase/5-lipoxygenase inhibitor. Eur J Pharmacol; 2009 Apr 1;607(1-3):244-50
Hazardous Substances Data Bank. CARRAGEENAN GUM .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Compound ZLJ-6 [(Z)-1-methyl-1,5-dihydro-2-amino-5-[4-(mesyl)benzylidene]-4H-imi-dazole-4-one mesilate] is a potent inhibitor of cyclooxygenase (IC(50)=0.73 and 0.31 microM, for cyclooxygenase-1 and cyclooxygenase-2 respectively) in human whole blood.
  • It also inhibited the production of thromboxane B(2) and prostaglandin E(2) in calcium ionophore A23187-induced human (IC(50)=0.50 microM) and rat whole blood (IC(50)=0.93 microM), and rat peritoneal leukocytes (IC(50)=2.27 microM).
  • ZLJ-6 suppressed the activity of 5-lipoxygenase in the rat basophilic leukemia (RBL-1) cell lysate (IC(50)=0.32 microM) and in intact cells (IC(50)=1.06 microM) and reduced the generation of leukotriene B(4) (LTB(4)) in A23187-stimulated human (IC(50)=1.61 microM) or rat whole blood (IC(50)=0.99 microM), and rat peritoneal leukocytes (IC(50)=2.59 microM).
  • In vivo, ZLJ-6, administered orally, demonstrated potent anti-inflammatory activity in the carrageenin-induced paw oedema model in rats and showed analgesic activity in the acetic acid-induced abdominal construction model in mice.
  • Thus ZLJ-6 is an ideal substitute for classical non-steroidal anti-inflammatory therapy.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Cyclooxygenase Inhibitors / pharmacology. Edema / drug therapy. Imidazoles / pharmacology. Sulfones / pharmacology
  • [MeSH-minor] Administration, Oral. Animals. Carrageenan. Cyclooxygenase 1 / drug effects. Cyclooxygenase 1 / metabolism. Cyclooxygenase 2 / drug effects. Cyclooxygenase 2 / metabolism. Dinoprostone / antagonists & inhibitors. Disease Models, Animal. Female. Humans. Inhibitory Concentration 50. Leukocytes / drug effects. Leukocytes / metabolism. Leukotriene B4 / antagonists & inhibitors. Lipoxygenase Inhibitors / administration & dosage. Lipoxygenase Inhibitors / pharmacology. Lipoxygenase Inhibitors / toxicity. Male. Rats. Rats, Sprague-Dawley. Thromboxane B2 / antagonists & inhibitors

  • MedlinePlus Health Information. consumer health - Edema.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19243697.001).
  • [ISSN] 1879-0712
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 1-methyl-1,5-dihydro-2-amino-5-(4-(mesyl)benzylidene)-4H-imidazole-4-one; 0 / Anti-Inflammatory Agents; 0 / Cyclooxygenase Inhibitors; 0 / Imidazoles; 0 / Lipoxygenase Inhibitors; 0 / Sulfones; 1HGW4DR56D / Leukotriene B4; 54397-85-2 / Thromboxane B2; 9000-07-1 / Carrageenan; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
  •  go-up   go-down


20. Baroody FM, Naclerio RM: Antiallergic effects of H1-receptor antagonists. Allergy; 2000;55 Suppl 64:17-27
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The primary mechanism of antihistamine action in the treatment of allergic diseases is believed to be competitive antagonism of histamine binding to cellular receptors (specifically, the H1-receptors), which are present on nerve endings, smooth muscles, and glandular cells.
  • This notion is supported by the fact that structurally unrelated drugs antagonize the H1-receptor and provide clinical benefit.
  • However, H1-receptor antagonism may not be their sole mechanism of action in treating allergic rhinitis.
  • On the basis of in vitro and animal experiments, drugs classified as H1-receptor antagonists have long been recognized to have additional pharmacological properties.
  • These additional properties are not uniformly distributed among drugs classified as H1-receptor antagonists.
  • In human challenge models, terfenadine, azatadine, and loratadine reduce IgE-mediated histamine release.
  • Cetirizine reduces eosinophilic infiltration at the site of antigen challenge in the skin, but not the nose.
  • In a nasal antigen challenge model, cetirizine pretreatment did not affect the levels of histamine and prostaglandin D2 recovered in postchallenge lavages, whereas the levels of albumin, N-tosyl-L-arginine methyl ester (TAME) esterase activity, and LTs were reduced.
  • In animal models, mizolastine inhibits antigen-induced eosinophil infiltration into mouse skin and into the nasal cavity of guinea-pigs.
  • Mizolastine also significantly inhibits antigen-induced neutrophil infiltration into the bronchoalveolar lavage fluids of guinea-pigs.
  • In man, mizolastine inhibits early and late antigen-induced soluble intercellular adhesion molecule 1 (ICAM-1) levels in skin blisters.
  • It also inhibits anaphylactic release of histamine from rodent mast cells, LTC4 and LTB4 release from mouse bone-marrow-derived mast cells, LTC4 release from rat intestinal mast cells, and 5-lipoxygenase activity of polymorphonuclear neutrophils of guinea-pig intestines and rat basophilic leukaemia cells.
  • It is equally clear that these antiallergic effects are not uniformly shared among all drugs of this class.
  • The assessment of the clinical significance of these results and research regarding the parts of the molecules responsible for these activities are underway.
  • [MeSH-major] Anti-Allergic Agents / immunology. Histamine H1 Antagonists / immunology. Histamine H1 Antagonists / therapeutic use. Hypersensitivity / drug therapy. Hypersensitivity / immunology
  • [MeSH-minor] Animals. Benzimidazoles / immunology. Benzimidazoles / therapeutic use. Disease Models, Animal. Humans. Receptors, Histamine H1 / immunology. Rhinitis / drug therapy. Rhinitis / immunology

  • MedlinePlus Health Information. consumer health - Allergy.
  • SciCrunch. DrugBank: Data: Chemical .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11291777.001).
  • [ISSN] 0105-4538
  • [Journal-full-title] Allergy
  • [ISO-abbreviation] Allergy
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI45583; United States / NIDCD NIH HHS / DC / DC 02714
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Allergic Agents; 0 / Benzimidazoles; 0 / Histamine H1 Antagonists; 0 / Receptors, Histamine H1; 244O1F90NA / mizolastine
  • [Number-of-references] 34
  •  go-up   go-down


21. Song Y, Qu C, Srivastava K, Yang N, Busse P, Zhao W, Li XM: Food allergy herbal formula 2 protection against peanut anaphylactic reaction is via inhibition of mast cells and basophils. J Allergy Clin Immunol; 2010 Dec;126(6):1208-17.e3
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, the mechanisms underlying this effect are not fully elucidated.
  • OBJECTIVE: To investigate whether FAHF-2 inhibits mast cell/basophil numbers and IgE-mediated activation.
  • METHODS: Mice with peanut allergy (PNA mice) were treated with FAHF-2 intragastrically for 7 weeks and challenged intragastrically with peanut 1 day and 4 weeks posttreatment.
  • Peripheral blood basophil numbers and peritoneal mast cell numbers and FcεRI expression were determined.
  • Direct effects of FAHF-2 on the murine mast cell line MC/9, and effects of 4 fractions and 3 compounds isolated from FAHF-2 on rat basophilic leukemia cells (RBL-2H3) and human skin mast cells degranulation and on the IgE-mediated spleen tyrosine kinase signaling pathway, were determined.
  • RESULTS: Although all sham-treated PNA mice developed anaphylaxis, FAHF-2-treated PNA mice were protected against anaphylaxis after peanut challenge at 1 day and 4 weeks posttherapy.
  • Reduction of peripheral blood basophils began after 1 week of treatment and continued for at least 4 weeks posttherapy.
  • Fraction 2 from FAHF-2 inhibited RBL-2H3 cell and human mast cell degranulation.

  • MedlinePlus Health Information. consumer health - Food Allergy.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
  • [Cites] Curr Opin Hematol. 2000 Jan;7(1):32-9 [10608502.001]
  • [Cites] Biochem Biophys Res Commun. 2010 May 14;395(4):547-52 [20394728.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1616-7 [10979667.001]
  • [Cites] APMIS. 2000 Oct;108(10):633-41 [11200817.001]
  • [Cites] J Allergy Clin Immunol. 2001 Jun;107(6):1077-81 [11398088.001]
  • [Cites] Immunity. 2001 Jun;14(6):791-800 [11420048.001]
  • [Cites] Immunity. 2001 Jun;14(6):801-11 [11420049.001]
  • [Cites] J Allergy Clin Immunol. 2001 Aug;108(2 Suppl):S84-8 [11498678.001]
  • [Cites] J Allergy Clin Immunol. 2001 Oct;108(4):639-46 [11590394.001]
  • [Cites] J Allergy Clin Immunol. 2002 Jul;110(1):117-24 [12110830.001]
  • [Cites] Nat Rev Immunol. 2002 Oct;2(10):773-86 [12360215.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12911-6 [14569021.001]
  • [Cites] J Immunol. 2004 Oct 1;173(7):4317-23 [15383560.001]
  • [Cites] J Exp Med. 1997 Feb 17;185(4):663-72 [9034145.001]
  • [Cites] J Immunol. 1997 Mar 15;158(6):2517-21 [9058781.001]
  • [Cites] J Allergy Clin Immunol. 2005 Jan;115(1):171-8 [15637565.001]
  • [Cites] J Immunol. 2005 Aug 15;175(4):2635-42 [16081839.001]
  • [Cites] Clin Exp Allergy. 2007 May;37(5):651-60 [17456212.001]
  • [Cites] Clin Exp Allergy. 2007 Jun;37(6):846-55 [17517098.001]
  • [Cites] Clin Exp Allergy. 2007 Sep;37(9):1392-403 [17845421.001]
  • [Cites] J Med Food. 2008 Mar;11(1):14-20 [18361733.001]
  • [Cites] Phytother Res. 2008 May;22(5):651-9 [18389474.001]
  • [Cites] J Agric Food Chem. 2008 Dec 24;56(24):12073-80 [19053379.001]
  • [Cites] J Allergy Clin Immunol. 2009 Feb;123(2):443-51 [19203662.001]
  • [Cites] Food Chem Toxicol. 2009 Jul;47(7):1659-66 [19394399.001]
  • [Cites] Inflamm Res. 2009 Sep;58(9):611-8 [19301096.001]
  • [Cites] Curr Opin Hematol. 2010 Jan;17(1):60-6 [19741522.001]
  • [Cites] J Allergy Clin Immunol. 2000 Jul;106(1 Pt 1):150-8 [10887318.001]
  • (PMID = 21134573.001).
  • [ISSN] 1097-6825
  • [Journal-full-title] The Journal of allergy and clinical immunology
  • [ISO-abbreviation] J. Allergy Clin. Immunol.
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / AT001495-05A1; United States / NCCIH NIH HHS / AT / R01 AT001495; United States / NCCIH NIH HHS / AT / R01 AT001495-05A1; United States / NCCIH NIH HHS / AT / AT001495-01A1; United States / NCCIH NIH HHS / AT / 2 R01 AT001495-05A1; United States / NCCIH NIH HHS / AT / R01 AT001495-01A1; United States / NCCIH NIH HHS / AT / 1R01AT001495-01A1
  • [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 / Food Allergy Herbal Formula-2; 0 / Plant Extracts; 0 / Receptors, IgE; 37341-29-0 / Immunoglobulin E
  • [Other-IDs] NLM/ NIHMS248602; NLM/ PMC3059770
  •  go-up   go-down


22. Melgarejo E, Medina MA, Sánchez-Jiménez F, Urdiales JL: Targeting of histamine producing cells by EGCG: a green dart against inflammation? J Physiol Biochem; 2010 Sep;66(3):265-70
Hazardous Substances Data Bank. HISTAMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The human body is made of some 250 different cell types.
  • From them, only a small subset of cell types is able to produce histamine.
  • In spite of the reduced number of these histamine-producing cell types, they are involved in very different physiological processes.
  • Their deregulation is related with many highly prevalent, as well as emergent and rare diseases, mainly those described as inflammation-dependent pathologies, including mastocytosis, basophilic leukemia, gastric ulcer, Crohn disease, and other inflammatory bowel diseases.
  • This is the case of melanoma, small cell lung carcinoma, and several types of neuroendocrine tumors.
  • In fact, EGCG has been shown to have potent anti-inflammatory, anti-tumoral, and anti-angiogenic effects and to be a potent inhibitor of the histamine-producing enzyme, histidine decarboxylase.
  • Herein, we review the many specific effects of EGCG on concrete molecular targets of histamine-producing cells and discuss the relevance of these data to support the potential therapeutic interest of this compound to treat inflammation-dependent diseases.
  • [MeSH-major] Catechin / analogs & derivatives. Histamine / biosynthesis. Inflammation / drug therapy
  • [MeSH-minor] Anti-Inflammatory Agents / metabolism. Basophils / drug effects. Humans. Macrophages / drug effects. Megakaryocytes / drug effects. Monocytes / drug effects. Neurons / drug effects. Tea / chemistry

  • Hazardous Substances Data Bank. Green tea .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cardiovasc Hematol Disord Drug Targets. 2007 Jun;7(2):135-44 [17584048.001]
  • [Cites] J Am Coll Nutr. 2006 Apr;25(2):79-99 [16582024.001]
  • [Cites] Monogr Allergy. 1978;13:1-113 [362171.001]
  • [Cites] J Immunol. 2004 Nov 1;173(9):5794-800 [15494532.001]
  • [Cites] Curr Opin Immunol. 1997 Dec;9(6):851-7 [9492989.001]
  • [Cites] Nutrition. 2002 May;18(5):443-4 [11985958.001]
  • [Cites] Arthritis Rheum. 2002 Aug;46(8):2079-86 [12209512.001]
  • [Cites] Cell Mol Life Sci. 2003 Aug;60(8):1760-3 [14521154.001]
  • [Cites] Cancer Causes Control. 1998 Mar;9(2):209-16 [9578298.001]
  • [Cites] J Nutr Biochem. 2010 Jul;21(7):659-64 [19616927.001]
  • [Cites] Neurosignals. 2005;14(1-2):46-60 [15956814.001]
  • [Cites] J Nutr. 1998 Dec;128(12):2334-40 [9868178.001]
  • [Cites] Cell Mol Life Sci. 2007 Oct;64(19-20):2690-701 [17878996.001]
  • [Cites] Nature. 1997 Jun 5;387(6633):561 [9177339.001]
  • [Cites] J Invest Dermatol. 2008 Oct;128(10 ):2429-41 [18463684.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Dec 7;364(1):79-85 [17927962.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):700-13 [12359210.001]
  • [Cites] Prog Neurobiol. 2007 Aug;82(6):348-60 [17659826.001]
  • [Cites] PLoS One. 2007 Nov 07;2(11):e1153 [17987129.001]
  • [Cites] Biochem Biophys Res Commun. 2009 Feb 20;379(4):1033-7 [19150340.001]
  • [Cites] Mol Cancer Ther. 2005 Jan;4(1):81-90 [15657356.001]
  • [Cites] Arch Biochem Biophys. 2000 Apr 15;376(2):338-46 [10775421.001]
  • [Cites] Free Radic Biol Med. 2008 Mar 15;44(6):1032-41 [18206666.001]
  • [Cites] Free Radic Biol Med. 2006 Aug 15;41(4):549-56 [16863987.001]
  • [Cites] J Biomed Sci. 2003 Mar-Apr;10(2):219-27 [12595758.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Sep 22;348(2):524-31 [16889749.001]
  • [Cites] J Radiat Res. 2006 Jun;47(2):213-20 [16819147.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Apr 9;316(3):659-65 [15033450.001]
  • [Cites] Am J Med. 1999 May 31;106(5B):37S-42S [10390126.001]
  • [Cites] J Rheumatol. 2005 Oct;32(10):1958-67 [16206353.001]
  • [Cites] Arch Biochem Biophys. 2008 Aug 15;476(2):133-8 [18358230.001]
  • [Cites] Cancer Lett. 1995 Nov 27;98(1):27-31 [8529202.001]
  • [Cites] Prev Med. 1992 May;21(3):334-50 [1614995.001]
  • [Cites] J Oral Pathol Med. 2007 Nov;36(10):588-93 [17944751.001]
  • [Cites] Chem Pharm Bull (Tokyo). 1988 Jan;36(1):227-33 [3378286.001]
  • [Cites] Arch Biochem Biophys. 2003 Feb 1;410(1):177-85 [12559991.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Jan 11;365(2):310-5 [17996193.001]
  • [Cites] Br J Pharmacol. 2009 Dec;158(7):1705-12 [19912233.001]
  • [Cites] FASEB J. 2001 May;15(7):1309-11 [11344123.001]
  • [Cites] Crit Rev Biochem Mol Biol. 2003;38(1):23-59 [12641342.001]
  • [Cites] Mutat Res. 2003 Feb-Mar;523-524:119-25 [12628509.001]
  • [Cites] World J Gastroenterol. 2007 Feb 28;13(8):1162-9 [17451194.001]
  • [Cites] J Cell Biochem Suppl. 1997;27:68-75 [9591195.001]
  • [Cites] J Allergy Clin Immunol. 2005 Jan;115(1):186-91 [15637567.001]
  • [Cites] Arthritis Rheum. 2006 Aug;54(8):2393-401 [16869002.001]
  • [Cites] Mol Pharmacol. 2010 Jan;77(1):17-25 [19828731.001]
  • [Cites] J Agric Food Chem. 2001 May;49(5):2527-31 [11368631.001]
  • [Cites] J Agric Food Chem. 2002 Sep 25;50(20):5729-34 [12236706.001]
  • [Cites] Atherosclerosis. 2000 Jan;148(1):67-73 [10580172.001]
  • [Cites] J Agric Food Chem. 2003 Mar 26;51(7):1858-63 [12643642.001]
  • [Cites] Biochem Pharmacol. 2001 Nov 1;62(9):1175-83 [11705450.001]
  • [Cites] Chem Biol Interact. 2008 Jan 10;171(1):89-95 [17931610.001]
  • [Cites] J Agric Food Chem. 2007 Jan 24;55(2):299-304 [17227057.001]
  • [Cites] Int Immunopharmacol. 2002 May;2(6):849-55 [12095176.001]
  • [Cites] Mol Carcinog. 2006 May;45(5):309-19 [16508969.001]
  • [Cites] Nat Struct Mol Biol. 2004 Apr;11(4):380-1 [15024383.001]
  • [Cites] Mutat Res. 2003 Feb-Mar;523-524:201-8 [12628518.001]
  • [Cites] J Am Coll Nutr. 2002 Feb;21(1):1-13 [11838881.001]
  • [Cites] Ann N Y Acad Sci. 2002 Nov;973:435-7 [12485906.001]
  • [Cites] Free Radic Res Commun. 1987;2(4-6):289-94 [3504810.001]
  • [Cites] Nature. 1999 Apr 1;398(6726):381 [10201368.001]
  • [Cites] J Cell Biochem Suppl. 1997;27:59-67 [9591194.001]
  • [Cites] J Hypertens. 1999 Apr;17(4):457-63 [10404946.001]
  • [Cites] Biol Pharm Bull. 1995 Jul;18(7):1006-8 [7581239.001]
  • [Cites] Biochem Pharmacol. 1997 Dec 15;54(12):1281-6 [9393670.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Aug 11;274(3):603-8 [10924324.001]
  • [Cites] Am J Clin Nutr. 2005 Jan;81(1 Suppl):284S-291S [15640492.001]
  • (PMID = 20652470.001).
  • [ISSN] 1138-7548
  • [Journal-full-title] Journal of physiology and biochemistry
  • [ISO-abbreviation] J. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Tea; 820484N8I3 / Histamine; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate
  •  go-up   go-down


23. Giagounidis AA, Hildebrandt B, Heinsch M, Germing U, Aivado M, Aul C: Acute basophilic leukemia. Eur J Haematol; 2001 Aug;67(2):72-6
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute basophilic leukemia.
  • Acute basophilic leukemia has recently been included into a revised classification of acute leukemias proposed by the WHO panel.
  • Due to the rarity of the disease, consistent diagnostic criteria are lacking.
  • We report on two cases of acute basophilic leukemia that occurred in our department during the last 10 yr.
  • Both patients were >60 yr of age, and presented in good clinical condition with alterations to their full blood count.
  • Cytogenetic analyses in the first patient showed a normal karyotype, while the second displayed a translocation t(2;6); (q23?4;p22?3), as well as a del (12)(p11).
  • Earlier observations have linked bone marrow basophilia either to a deletion of the short arm of chromosome 12 (p11-13), to translocations involving the long arm of chomosome 6 at 6q23 or to the translocation t(6,9); (p23;q34).
  • However, other translocations involving chromosome 6p23 have not been described before.
  • Treatment of our patients consisted of supportive treatment in the one with normal karyotype and aggressive chemotherapy in the other patient.
  • Both patients died within one year after diagnosis due to progressive or recurrent leukemia.
  • [MeSH-major] Leukemia, Basophilic, Acute / diagnosis
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations. Coloring Agents. Cytarabine / administration & dosage. Cytoplasmic Granules / chemistry. Fatal Outcome. Humans. Idarubicin / administration & dosage. Immunophenotyping. Karyotyping. Leukocyte Count. Male. Middle Aged. Neoplasm Proteins / analysis. Neoplastic Stem Cells / chemistry. Neoplastic Stem Cells / pathology. Periodic Acid-Schiff Reaction. Peroxidase / analysis. Recurrence. Tolonium Chloride. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11722593.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Neoplasm Proteins; 04079A1RDZ / Cytarabine; 15XUH0X66N / Tolonium Chloride; EC 1.11.1.7 / Peroxidase; ZRP63D75JW / Idarubicin
  •  go-up   go-down






Advertisement