| Inorganic mercury dissociates preassembled Fas/CD95 receptor oligomers in T lymphocytes. | |
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MedLine Citation:
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PMID: 16039944 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Genetically susceptible rodents exposed to low burdens of inorganic mercury (Hg2+) develop autoimmune disease. Previous studies have shown that low, noncytotoxic levels of Hg2+ inhibit Fas-mediated apoptosis in T cells. These results suggest that inhibition of the Fas death receptor pathway potentially contributes to autoimmune disease after Hg2+ exposure, as a consequence of disruption of peripheral tolerance. The formation of active death inducing signaling complexes (DISC) following CD95/Fas receptor oligomerization is a primary step in the Fas-mediated apoptotic pathway. Other recent studies have shown that Hg2+ at concentrations that inhibit apoptosis also inhibit formation of active DISC, suggesting that inhibition of DISC is the mechanism responsible for Hg2+-mediated inhibition of apotosis. Preassociated Fas receptors have been implicated as key elements necessary for the production of functional DISC. We present evidence in this study showing that low and nontoxic concentrations of Hg2+ induce the dissociation of preassembled Fas receptor complexes in Jurkat T cells. Thus, this Hg2+-induced event should subsequently decrease the amount of preassembled Fas available for DISC formation, potentially resulting in the attenuation of Fas-mediated apoptosis in T lymphocytes. |
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Authors:
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Stamatina E Ziemba; Michael J McCabe; Allen J Rosenspire |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S. Date: 2005-01-08 |
Journal Detail:
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Title: Toxicology and applied pharmacology Volume: 206 ISSN: 0041-008X ISO Abbreviation: Toxicol. Appl. Pharmacol. Publication Date: 2005 Aug |
Date Detail:
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Created Date: 2005-07-25 Completed Date: 2005-09-15 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0416575 Medline TA: Toxicol Appl Pharmacol Country: United States |
Other Details:
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Languages: eng Pagination: 334-42 Citation Subset: IM |
Affiliation:
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Department of Biological Sciences, Wayne State University, 5047 Gullen Mall, Detroit, MI 48202, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antigens, CD95
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metabolism* Biopolymers Blotting, Western Chlorides / pharmacology Death Domain Receptor Signaling Adaptor Proteins Electrophoresis, Polyacrylamide Gel Environmental Pollutants / toxicity* Humans Jurkat Cells Mercuric Chloride / toxicity* Receptors, Tumor Necrosis Factor / metabolism T-Lymphocytes / drug effects*, metabolism Zinc Compounds / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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P30 ES01247/ES/NIEHS NIH HHS; R01 ES012403/ES/NIEHS NIH HHS; R01 ES11000/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD95; 0/Biopolymers; 0/Chlorides; 0/Death Domain Receptor Signaling Adaptor Proteins; 0/Environmental Pollutants; 0/Receptors, Tumor Necrosis Factor; 0/Zinc Compounds; 7487-94-7/Mercuric Chloride; 7646-85-7/zinc chloride |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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