کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5844003 | 1127496 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Phosphoprotein enriched in astrocytes (PEA)-15: A potential therapeutic target in multiple disease states
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کلمات کلیدی
PLD1TGF-β1VSMPEA-15RSKHNF-4αDEDPCOSPDGFGLUTCaMKIIFADDDISCPKCERK1/2 - ERK1 / 2Ribosomal s6 kinase - s6 کیناز ریبوزومیinterleukin - اینترلوکینTransforming growth factor-β1 - تبدیل فاکتور رشد β1Proliferation - ترویجGlucose transporter - حمل و نقل گلوکزApoptosis - خزان یاختهایdeath effector domain - دامنه موثر مرگType 2 diabetes - دیابت نوع 2Cancer - سرطانNSCLC - سرطان ریوی غیر سلول کوچکNon-small cell lung cancer - سرطان غیر سلول کوچک ریهPolycystic ovary syndrome - سندرم تخمدان پلی کیستیکVascular smooth muscle - عضله صاف عضلانیplatelet-derived growth factor - فاکتور رشد حاصل از پلاکتPhospholipase D1 - فسفولیپاز D1TRAIL - قطارtumour necrosis factor-related apoptosis-inducing ligand - لیگاند ناشی از آپوپتوز وابسته به عامل بیماری تومورmap - نقشهFAS-associated death domain protein - پروتئین دامنه مرگ مرتبط با FASmitogen-activated protein - پروتئین فعال mitogencalcium/calmodulin-dependent protein kinase II - پروتئین کیناز II وابسته به کلسیم / کالودولینProtein kinase C - پروتئین کیناز سیExtracellular signal-regulated kinases 1/2 - کینازهای تنظیم شده سیگنال غیر سلولی 1/2
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
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چکیده انگلیسی
Phosphoprotein enriched in astrocytes-15 (PEA-15) is a cytoplasmic protein that sits at an important junction in intracellular signalling and can regulate diverse cellular processes, such as proliferation and apoptosis, dependent upon stimulation. Regulation of these processes occurs by virtue of the unique interaction of PEA-15 with other signalling proteins. PEA-15 acts as a cytoplasmic tether for the mitogen-activated protein kinases, extracellular signal-regulated kinase 1/2 (ERK1/2) preventing nuclear localisation. In order to release ERK1/2, PEA-15 requires to be phosphorylated via several potential pathways. PEA-15 (and its phosphorylation state) therefore regulates many ERK1/2-dependent processes, including proliferation, via regulating ERK1/2 nuclear translocation. In addition, PEA-15 contains a death effector domain (DED) which allows interaction with other DED-containing proteins. PEA-15 can bind the DED-containing apoptotic adaptor molecule, Fas-associated death domain protein (FADD) which is also dependent on the phosphorylation status of PEA-15. PEA-15 binding of FADD can inhibit apoptosis as bound FADD cannot participate in the assembly of apoptotic signalling complexes. Through these protein-protein interactions, PEA-15-regulated cellular effects have now been investigated in a number of disease-related studies. Changes in PEA-15 expression and regulation have been observed in diabetes mellitus, cancer, neurological disorders and the cardiovascular system. These changes have been suggested to contribute to the pathology related to each of these disease states. As such, new therapeutic targets based around PEA-15 and its associated interactions are now being uncovered and could provide novel avenues for treatment strategies in multiple diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacology & Therapeutics - Volume 143, Issue 3, September 2014, Pages 265-274
Journal: Pharmacology & Therapeutics - Volume 143, Issue 3, September 2014, Pages 265-274
نویسندگان
Fiona H. Greig, Graeme F. Nixon,