کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8475033 | 1550442 | 2013 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Posttranslational modifications of cardiac troponin T: An overview
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کلمات کلیدی
ROCK-IIPTMPP1GFCCAMK IIASK1AmI - AMICa2 +/calmodulin-dependent protein kinase II - Ca2 + / calmodulin وابسته پروتئین کیناز IIposttranslational modification - اصلاح posttranslationalright ventricle - بطن راستleft ventricle - بطن چپESRD یا end stage renal disease - بیماری کلیوی در مرحله نهایی End-stage renal disease - بیماری کلیوی در مرحله پایانیTropomyosin - تروپومیوسینcardiac troponin T - تروپونین T قلبFragmentation - تقسیم بندیAcute myocardial infarction - سکته قلبیMass spectrometry - طیف سنجی جرمیinorganic phosphate - فسفات معدنیPhosphorylation - فسفریلاسیونCardiac physiology - فیزیولوژی قلبheart failure - نارسایی قلبیgel filtration chromatography - کروماتوگرافی تصفیه ژلapoptosis signal-regulating kinase 1 - کیناز تنظیم کننده سیگنال آپوپتوز 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Cardiac troponin (cTn) is an important sarcomeric protein complex situated on the thin filament and is involved in the regulation of cardiac muscle contraction. This regulation is primarily controlled by Ca2Â + binding to troponin C and in addition fine-tuned by the posttranslational modification of cTnI and cTnT. The vast majority of cTnT modifications involve the phosphorylation by protein kinase C (PKC) or other kinases and the N-terminal cleavage by caspase and calpain. In vitro studies employing reconstituted detergent-skinned fiber bundles and cell culture generally show a detrimental effect of cTnT phosphorylation on muscle contraction, which is backed by some in vivo studies finding increased cTnT phosphorylation in heart failure, but contradicted by others. In addition, N-terminal cleavage of cTnT is thought to be another factor influencing cardiac contraction. Time-dependent degradation of cTnT has been observed in human serum upon myocardial infarction. These molecular changes might influence the immunoreactivity of cTnT in the clinical immunoassay and have consequences for the clinical interpretations of these measurements. No consensus has yet been reached on the occurrence and extent of these observations and their underlying processes are subject of intense scientific debate. This review will focus on discussing these modifications, their implications on physiology and disease and summarizes the complex interplays of different enzymes on the molecular forms of cTnT and their associated effects.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 63, October 2013, Pages 47-56
Journal: Journal of Molecular and Cellular Cardiology - Volume 63, October 2013, Pages 47-56
نویسندگان
Alexander S. Streng, Douwe de Boer, Jolanda van der Velden, Marja P. van Dieijen-Visser, Will K.W.H. Wodzig,