کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10816539 | 1058577 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of the extracellular signal-regulated kinase pathway in adult myocardium: differential roles of Gq/11, Gi and G12/13 proteins in signalling by α1-adrenergic, endothelin-1 and thrombin-sensitive protease-activated receptors
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کلمات کلیدی
JnkNRVMARVMp90RSKPAR-1c-Jun NH2-terminal kinasePKBET-1GPCRERKeGFPCPAMAPK - MAPKMOI - MENeonatal rat ventricular myocytes - myocytes بطن چپ نوزادendothelin-1 - اندوتلین-1Cyclopentyladenosine - سیکلوپنتیلادنوزینadult rat ventricular myocytes - میوکسی های بطنی بالغ رتenhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استprotein kinase B - پروتئین کیناز Bmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenmultiplicity of infection - چندین عفونتextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیProtease-activated receptor-1 - گیرنده پروتئاز فعال شده-1G protein-coupled receptor - گیرندههای جفتشونده با پروتئین جی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Regulation of the extracellular signal-regulated kinase pathway in adult myocardium: differential roles of Gq/11, Gi and G12/13 proteins in signalling by α1-adrenergic, endothelin-1 and thrombin-sensitive protease-activated receptors Regulation of the extracellular signal-regulated kinase pathway in adult myocardium: differential roles of Gq/11, Gi and G12/13 proteins in signalling by α1-adrenergic, endothelin-1 and thrombin-sensitive protease-activated receptors](/preview/png/10816539.png)
چکیده انگلیسی
Using adenoviruses encoding RGS2, RGS4 and Lsc (regulator of G protein signalling (RGS) domain of p115 RhoGEF), we investigated the contributions of Gq/11, Gi and G12/13 proteins to G protein-coupled receptor (GPCR)-mediated activation of the extracellular signal-regulated kinase (ERK) pathway in adult rat ventricular myocytes (ARVM). Exposure to phenylephrine, endothelin-1 (ET-1) or thrombin induced significant activation of ERK1/2 and their downstream target 90 kDa ribosomal S6 kinase (p90RSK), which was abolished by overexpression of RGS4 (inhibits signalling via Gq/11 and Gi) or RGS2 (inhibits signalling via Gq/11). Pertussis toxin (inhibits signalling via Gi) only partially attenuated the activation of ERK1/2 and p90RSK by phenylephrine and ET-1, but abolished such activation by thrombin. Overexpression of Lsc (inhibits signalling via G12/13) did not affect the responses to phenylephrine and ET-1, but suppressed the activation of ERK1/2 and p90RSK by thrombin. We conclude that full activation of the ERK pathway in ARVM by α1-adrenergic, ET-1 and thrombin receptors requires the activation of distinct families of heterotrimeric G proteins.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 17, Issue 5, May 2005, Pages 655-664
Journal: Cellular Signalling - Volume 17, Issue 5, May 2005, Pages 655-664
نویسندگان
Andrew K. Snabaitis, Andreas Muntendorf, Thomas Wieland, Metin Avkiran,