کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10816344 | 1058564 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The conditional kinase ÎMEKK1:ER* selectively activates the JNK pathway and protects against serum withdrawal-induced cell death
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کلمات کلیدی
4-hydroxytamoxifenMAPK or ERK kinase4-HTMEKKMEKK3Bcl-2 antagonist of cell deathSB203580SAPKMEKK1U0126PKBNGFPI3KJnkERKFBSc-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKBAD - بدApoptosis - خزان یاختهایBcl-2 homology domain - دامنه هماهنگ Bcl-2fetal bovine serum - سرم جنین گاوnerve growth factor - فاکتور رشد عصبphosphatidylinositol 3′-kinase - فسفاتیدیلینواستیل 3'-kinaseMEK - مجاهدین خلقMEK kinase - مجله کینازBIM - مدلسازی اطلاعات ساختمانRibosomal protein S6 - پروتئین Ribosomal S6protein kinase B - پروتئین کیناز Bmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenStress-activated protein kinase - پروتئین کیناز فعال شده با استرسKinase - کینازextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The conditional protein kinase ÎMEKK3:ER* allows activation of the mitogen-activated and stress-activated protein kinases (MAPKs and SAPKs) without imposing a primary cellular stress or damage. Such separation of stress from stress-induced signalling is particularly important in the analysis of apoptosis. Activation of ÎMEKK3:ER* in cycling CCl39 cells caused a rapid stimulation of the ERK1/2, JNK and p38 pathways but resulted in a slow, delayed apoptotic response. Paradoxically, activation of the same pathways inhibited the rapid expression of BimEL and apoptosis following withdrawal of serum. Inhibition of the ERK1/2 pathway prevented the down-regulation of BimEL but caused only a partial reversion of the cyto-protective effect of ÎMEKK3:ER*. In contrast, inhibition of p38 had no effect, raising the possibility that activation of JNK might also exert a protective effect. To test this we used CCl39 cells expressing ÎMEKK1:ER* which activates JNK but not ERK1/2, p38, PKB or IκB kinase. Activation of ÎMEKK1:ER* inhibited serum withdrawal-induced conformational changes in Bax and apoptosis. These results suggest that in the absence of any overt cellular damage or chemical stress activation of JNK can act independently of the ERK1/2 or PKB pathways to inhibit serum withdrawal-induced cell death.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 17, Issue 11, November 2005, Pages 1412-1422
Journal: Cellular Signalling - Volume 17, Issue 11, November 2005, Pages 1412-1422
نویسندگان
Sarah A. Molton, Claire Weston, Kathryn Balmanno, Catherine Newson, Daniel E. Todd, Andrew P. Garner, Simon J. Cook,