کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278458 | 1295819 | 2007 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The role of poly(ADP-ribose) polymerase-1 in CNS disease
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کلمات کلیدی
NF-κBMPTPTNFαEAEMMP-9PARP-11-methyl 4-phenyl 1,2,3,6-tetrahydropyridine - 1-متیل 4-فنیل 1،2،3،6-تتراهیدروپیریدینDNA - DNA یا اسید دزوکسی ریبونوکلئیکNAD+ - NAD +experimental allergic encephalomyelitis - آنسفالومیلیت آلرژیک تجربیAIF - آیفونinflammation - التهاب( توروم) Oxidative stress - تنش اکسیداتیوtumor necrosis factor alpha - تومور نکروز عامل آلفاTranscription - رونویسیapoptosis-inducing factor - عامل القاء آپوپتوزnuclear factor κB - فاکتور هسته ای κBMatrix metalloproteinase-9 - ماتریکس متالوپروتئیناز -9Cell death - مرگ سلولی NAD, nicotinamide adenine dinucleotide - نیکوتینامید آدنین دینوکلئوتیدPoly(ADP-ribose) polymerase-1 - پلی (ADP-ribose) پلیمراز-1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme that contributes to both neuronal death and survival under stress conditions. PARP-1 is the most abundant of several PARP family members, accounting for more than 85% of nuclear PARP activity, and is present in all nucleated cells of multicellular animals. When activated by DNA damage, PARP-1 consumes nicotinamide adenine dinucleotide (NAD+) to form branched polymers of ADP-ribose on target proteins. This process can have at least three important consequences in the CNS, depending on the cell type and the extent of DNA damage: 1) Poly(ADP-ribose) formation on histones and on enzymes involved in DNA repair can prevent sister chromatid exchange and facilitate base-excision repair; 2) poly(ADP-ribose) formation can influence the action of transcription factors, notably nuclear factor κB, and thereby promote inflammation; and 3) extensive PARP-1 activation can promote neuronal death through mechanisms involving NAD+ depletion and release of apoptosis inducing factor from the mitochondria. PARP-1 activation is thereby a key mediator of neuronal death during excitotoxicity, ischemia, and oxidative stress, and PARP-1 gene deletion or pharmacological inhibition can markedly improve neuronal survival in these settings. PARP-1 activation has also been identified in Alzheimer's disease and in experimental allergic encephalitis, but the role of PARP-1 in these disorders remains to be established.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 145, Issue 4, 14 April 2007, Pages 1267-1272
Journal: Neuroscience - Volume 145, Issue 4, 14 April 2007, Pages 1267-1272
نویسندگان
T.M. Kauppinen, R.A. Swanson,