کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739055 | 1046858 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Redox response of the endogenous calcineurin inhibitor Adapt78
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کلمات کلیدی
PBSDPIDMEMFBSRNSNACN-acetylcysteine - N-استیل سیستئینROS - ROSHydrogen peroxide - آب اکسیژنهStress-response - استرس پاسخsodium dodecyl sulfate-polyacrylamide gel electrophoresis - الکتروفورز ژل دوده سولفات سدیم پلی آکریل آمیدSDS-PAGE - الکتروفورز ژل پلی آکریل آمیدOxidative stress - تنش اکسیداتیوDulbecco's minimal essential medium - حداقل کالای ضروری Dulbeccodiphenylene iodonium - دیوفنیلن یدونیومFree radicals - رادیکال آزادRedox - ردوکس(اکسایش و کاهش)fetal bovine serum - سرم جنین گاوcytoplasm - سیتوپلاسمPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریSubcellular localization - محلی سازی سلولT-cell response - پاسخ T-cellCalcineurin - کلسینورینreactive nitrogen species - گونه های واکنش پذیر نیتروژنReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Adapt78 (DSCR1/calcipressin/MCIP1) is a potent natural inhibitor of calcineurin, an important intracellular phosphatase that mediates many cellular responses to calcium. We previously reported two major cytosolic isoforms (1 and 4) of Adapt78, and that isoform 4 is an oxidative and calcium stress-response protein. Using a higher cell culture density and new antibody, we again observed that both major isoforms localized to the cytosol, but a significant level of isoform 4 (but not isoform 1) was also detected in the nucleus where it was present in the nonsoluble region and not associated with RNA. Exposure of cells to hydrogen peroxide led to the significant loss of isoform 4 from the nucleus with a moderate increase in cytosolic localization. The change in isoform 4 phosphorylation state in response to oxidative stress, characterized by a loss of the lesser (hypo) phosphorylated Adapt78, was not due to accelerated degradation, although general Adapt78 degradation was proteosome mediated. Finally, stimulation of Jurkat and primary T-lymphocyte signaling led to isoform 4 induction. This induction was BAPTA, diphenylene iodonium, and N-acetylcysteine inhibitable, and accompanied by induction of the classic immune response mediator and calcineurin-pathway-stimulated interleukin-2. These studies reveal new redox-related activities for Adapt78 isoform 4, which may contribute to its known calcineurin-regulating and cytoprotective activities, and further suggest that Adapt78 plays a role in basic T-cell response.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 6, 15 September 2005, Pages 719-727
Journal: Free Radical Biology and Medicine - Volume 39, Issue 6, 15 September 2005, Pages 719-727
نویسندگان
Ananth V. Narayan, Rebecca Stadel, Amy B. Hahn, Dipti L. Bhoiwala, Geysha Cornielle, Erwin Sarazin, Issam Koleilat, Dana R. Crawford,