Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 390, Issue 4, Pages 1102-1105Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.10.076
Keywords
Calcineurin; KCNK18 protein; Immune system disease; Immunosuppressive agents; Lymphocytes
Categories
Funding
- Korean Government [KRF-2008-313-E00026, KRF-2006-005-J04204]
- KOSEF [R13-2005-012-01002-0]
- National Research Foundation of Korea [R13-2005-012-01002-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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In this review, we propose that TRESK background K+ channel could serve as a potential therapeutic target for T-cell mediated immune dysfunction. TRESK has many immune function-related properties. TRESK is abundantly expressed in the thymus, the spleen, and human leukemic T-lymphocytes. TRESK is highly activated by Ca2+, calcineurin, acetylcholine, and histamine which induce hypertrophy, whereas TRESK is inhibited by immunosuppressants, Such as cyclosporin A and FK506. Cyclosporine A and FK506 target the binding site of nuclear factor of activated T-cells (NFAT) to inhibit calcineurin. Interestingly, TRESK possesses an NFAT-like docking site that is present at its intracellular loop. Calcineurin has been found to interact with TRESK via specific NFAT-like docking site. When the T-cell is activated, calcineurin can bind to the NFAT-clocking site of TRESK. The activation of both TRESK and NFAT via Ca2+-calcineurin-NFAT/TRESK pathway could modulate the transcription of new genes in addition to regulating several aspects of T-cell function. (C) 2009 Elsevier Inc. All rights reserved.
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