کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10801964 | 1055649 | 2015 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
FKBP25 and FKBP38 regulate non-capacitative calcium entry through TRPC6
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
WCLPrPTBSTHBSSTIM1SOCETRPC6OAGTHRFK506ACDFKBPsFKBdIP3RsTRPCOrai1FKBP25FKBP381-Oleoyl-2-acetyl-glycerolIP3DTTADPCypermethrinCyPBSA - BSACYPs - CYPhepes buffered saline - hepes بافر شورinositol 1,4,5-trisphosphate - inositol 1،4،5-trisphosphate[Ca2+]c - [Ca2 +] cbovine serum albumin - آلبومین سرم گاوCSA - ایالات مؤتلفهٔ آمریکاImmunophilins - ایمونوفیلین هاTacrolimus - تاکرولیموسThrombin - ترومبین یا فاکتور II diacyl glycerol - دیسیل گلیسرولdithiothreitol - دیتیوتریتولDAG - روزCAM - ساخت به کمک کامپیوترcyclosporin A - سیکلوسپورین ACyclophilins - سیکلوفیلین هاrough endoplasmic reticulum - شبکیه اندوپلاسمی خشنSERCA - قلبwhole cell lysate - لسیات کل سلولStromal interaction molecule 1 - مولکول تعامل استروما 1CAN - می توانwild type - نوع وحشیStore-operated calcium entry - واردات کلسیم در فروشگاهPlatelets - پلاکت هاCalmodulin - کالمودولینTransient receptor potential channel - کانال بالقوه گیرنده گذراCaP - کلاه لبه دارCalcineurin - کلسینورینinositol 1,4,5-trisphosphate receptors - گیرنده های inositol 1،4،5-trisphosphate
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: FKBP25 and FKBP38 regulate non-capacitative calcium entry through TRPC6 FKBP25 and FKBP38 regulate non-capacitative calcium entry through TRPC6](/preview/png/10801964.png)
چکیده انگلیسی
Non-capacitative calcium entry (NCCE) contributes to cell activation in response to the occupation of G protein-coupled membrane receptors. Thrombin administration to platelets evokes the synthesis of diacylglycerol downstream of PAR receptor activation. Diacylglycerol evokes NCCE through activating TRPC3 and TRPC6 in human platelets. Although it is known that immunophilins interact with TRPCs, the role of immunophilins in the regulation of NCCE remains unknown. Platelet incubation with FK506, an immunophilin antagonist, reduced OAG-evoked NCCE in a concentration-dependent manner, an effect that was independent on the inactivation of calcineurin (CaN). FK506 was unable to reduce NCCE evoked by OAG in platelets from TRPC6â/â mice. In HEK-293 cells overexpressing TRPC6, currents through TRPC6 were altered in the presence of FK506. We have found interaction between FKBP38 and other FKBPs, like FKBP25, FKBP12, and FKBP52 that were not affected by FK506, as well as with calmodulin (CaM). FK506 modified the pattern of association between FKBP25 and TRPCs as well as impaired OAG-evoked TRPC3 and TRPC6 coupling in both human and mouse platelets. By performing biotinylation experiments we have elucidated that FKBP25 and FKBP38 might be found at different cellular location, the plasma membrane and the already described intracellular locations. Finally, FKBP25 and FKBP38 silencing significantly inhibits OAG-evoked NCCE in MEG-01 and HEK293 cells, while overexpression of FKBP38 does not modify NCCE in HEK293 cells. All together, these findings provide strong evidence for a role of immunophilins, including FKBP25 and FKBP38, in NCCE mediated by TRPC6.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1853, Issue 10, Part A, October 2015, Pages 2684-2696
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1853, Issue 10, Part A, October 2015, Pages 2684-2696
نویسندگان
Esther Lopez, Alejandro Berna-Erro, Gines M. Salido, Juan A. Rosado, Pedro C. Redondo,