کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6286525 | 1615397 | 2014 | 20 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Role of the ubiquitin-proteasome system in brain ischemia: Friend or foe?
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کلمات کلیدی
PRUMCAOAPVcdk5NMDAReIF2α3-MAGKAPGRP78TRPMATF4HECTDUBα-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acidNedd4UBAPI3 KUCHBCOubiquitin associated domainPSD-95PDIPSDERADtPANOSeNOSUblAMPAAMPAROGDN-methyl-d-aspartateNMDA15-deoxy-Δ12,14-Prostaglandin J2 - 15-deoxy-Δ12،14-پروستاگلاندین J23-methyladenine - 3-متیل آدنینAPC/C - APC / CMdm2 - MDM2PKR-like ER kinase - PK-like ER kinase[Ca2+]i - [Ca2 +] ianaphase-promoting complex/cyclosome - آنافاز تکاملی / cyclosomeDeubiquitinating enzymes - آنزیم های Deubiquitinatingendothelial NOS - اندوتلیال NOSmiddle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیER-Associated Degradation - تخریب ER-AssociatedPost-synaptic density - تراکم پسا سیناپسیCHOP - تکه کردنRing - حلقهUbiquitin-like domain - دامنه Ubiquitin مانندregulatory particle - ذرات مقرراتBlood–brain barrier - سد خونی مغزیBBB - سد خونی مغزیcyclin-dependent kinase-5 - سیکلین وابسته به کیناز 5endoplasmic reticulum - شبکه آندوپلاسمی eukaryotic initiation factor 2α - عامل آغاز کننده یوکاریوتی 2αintracellular Ca2+ concentration - غلظت Ca2 + داخل سلولیphosphoinositide 3-kinase - فسفینوزیتید 3-کینازactivating transcription factor 4 - فعال کردن عامل رونویسی 4tissue plasminogen activator - فعال کننده بافتی پلاسمینوژنMarks - مارک هاOxygen and glucose deprivation - محرومیت از اکسیژن و گلوکزtransient receptor potential melastatin - میلزین بالقوه گیرنده گذراnitric oxide synthase - نیتریک اکسید سنتازHerp - هرپglucose-regulated protein 78 - پروتئین تنظیم شده با گلوکز 78Protein disulphide isomerase - پروتئین دی سولفید ایزومرازguanylate kinase-associated protein - پروتئین مرتبط با گینیلات کینازPERK - پرکreally interesting new gene - ژن جدید واقعا جالبKainate - کیناتNMDA receptors - گیرنده NMDAAMPA receptors - گیرنده های AMPA
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The ubiquitin-proteasome system (UPS) is a catalytic machinery that targets numerous cellular proteins for degradation, thus being essential to control a wide range of basic cellular processes and cell survival. Degradation of intracellular proteins via the UPS is a tightly regulated process initiated by tagging a target protein with a specific ubiquitin chain. Neurons are particularly vulnerable to any change in protein composition, and therefore the UPS is a key regulator of neuronal physiology. Alterations in UPS activity may induce pathological responses, ultimately leading to neuronal cell death. Brain ischemia triggers a complex series of biochemical and molecular mechanisms, such as an inflammatory response, an exacerbated production of misfolded and oxidized proteins, due to oxidative stress, and the breakdown of cellular integrity mainly mediated by excitotoxic glutamatergic signaling. Brain ischemia also damages protein degradation pathways which, together with the overproduction of damaged proteins and consequent upregulation of ubiquitin-conjugated proteins, contribute to the accumulation of ubiquitin-containing proteinaceous deposits. Despite recent advances, the factors leading to deposition of such aggregates after cerebral ischemic injury remain poorly understood. This review discusses the current knowledge on the role of the UPS in brain function and the molecular mechanisms contributing to UPS dysfunction in brain ischemia with consequent accumulation of ubiquitin-containing proteins. Chemical inhibitors of the proteasome and small molecule inhibitors of deubiquitinating enzymes, which promote the degradation of proteins by the proteasome, were both shown to provide neuroprotection in brain ischemia, and this apparent contradiction is also discussed in this review.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Progress in Neurobiology - Volume 112, January 2014, Pages 50-69
Journal: Progress in Neurobiology - Volume 112, January 2014, Pages 50-69
نویسندگان
Margarida V. Caldeira, Ivan L. Salazar, Michele Curcio, Lorella M.T. Canzoniero, Carlos B. Duarte,