کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815957 | 1058530 | 2015 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
EGF stimulates the activation of EGF receptors and the selective activation of major signaling pathways during mitosis
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کلمات کلیدی
I-phasePI3KEGFM-phasePLC-γ1ERKEGFRERKs - ERK هاAkt - آکتImmunoprecipitation - تخریب ایمنیCell signaling - سیگنالینگ سلولیGAP - شکافepidermal growth factor - عامل رشد اپیدرمیphospholipase C-γ1 - فسفولیپاز C-γ1phosphoinositide 3-kinase - فسفینوزیتید 3-کینازMEK - مجاهدین خلقInterphase - میان چهر، اینترفازMitosis - میتوزGTPase-activating protein - پروتئین فعال GTPasemitogen-activated protein kinase kinase - پروتئین کیناز کیناز فعال Mitogen فعالCell cycle - چرخه سلولیextracellular signal-regulated kinases - کیناز های تنظیم شده سیگنال خارج سلولیEGF receptor - گیرنده EGFEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Mitosis and epidermal growth factor (EGF) receptor (EGFR) are both targets for cancer therapy. The role of EGFR signaling in mitosis has been rarely studied and poorly understood. The limited studies indicate that the activation of EGFR and downstream signaling pathways is mostly inhibited during mitosis. However, we recently showed that EGFR is phosphorylated in response to EGF stimulation in mitosis. Here we studied EGF-induced EGFR activation and the activation of major signaling pathways downstream of EGFR during mitosis. We showed that EGFR was strongly activated by EGF during mitosis as all the five major tyrosine residues including Y992, Y1045, Y1068, Y1086, and Y1173 were phosphorylated to a level similar to that in the interphase. We further showed that the activated EGFR is able to selectively activate some downstream signaling pathways while avoiding others. Activated EGFR is able to activate PI3K and AKT2, but not AKT1, which may be responsible for the observed effects of EGF against nocodazole-induced cell death. Activated EGFR is also able to activate c-Src, c-Cbl and PLC-γ1 during mitosis. However, activated EGFR is unable to activate ERK1/2 and their downstream substrates RSK and Elk-1. While it activated Ras, EGFR failed to fully activate Raf-1 in mitosis due to the lack of phosphorylation at Y341 and the lack of dephosphorylation at pS259. We conclude that contrary to the dogma, EGFR is activated by EGF during mitosis. Moreover, EGFR-mediated cell signaling is regulated differently from the interphase to specifically serve the needs of the cell in mitosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 27, Issue 3, March 2015, Pages 638-651
Journal: Cellular Signalling - Volume 27, Issue 3, March 2015, Pages 638-651
نویسندگان
Ping Wee, Huaiping Shi, Jennifer Jiang, Yuluan Wang, Zhixiang Wang,