کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474658 | 1550430 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
An integrated mechanism of cardiomyocyte nuclear Ca2Â + signaling
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کلمات کلیدی
E–CONMPhosphatidylinositol-4-phosphatePI4PIGF-1INMET-1InsP3PLCInsP3RRyRPIP2inositol 1,4,5-trisphosphate - inositol 1،4،5-trisphosphateAngiotensin II - آنژیوتانسین دوendothelin-1 - اندوتلین-1insulin-like growth factor-1 - انسولین مانند عامل رشد 1excitation–contraction - تحریک-انقباضAng II - دومSarcoplasmic reticulum - رتیکولوم سارکوپلاسمیکendoplasmic reticulum - شبکه آندوپلاسمی Outer nuclear membrane - غشای هسته بیرونیInner nuclear membrane - غشای هسته داخلیphosphatidylinositol bisphosphate - فسفاتیدیلینوزیتول بیسفسفاتphospholipase C - فسفولیپاز CCardiomyocyte - قلب و عروقnuclear envelope - پاکت هسته ایInsP3 receptor - گیرنده InsP3Ryanodine receptor - گیرنده رایانودین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In cardiomyocytes, Ca2Â + plays a central role in governing both contraction and signaling events that regulate gene expression. Current evidence indicates that discrimination between these two critical functions is achieved by segregating Ca2Â + within subcellular microdomains: transcription is regulated by Ca2Â + release within nuclear microdomains, and excitation-contraction coupling is regulated by cytosolic Ca2Â +. Accordingly, a variety of agonists that control cardiomyocyte gene expression, such as endothelin-1, angiotensin-II or insulin-like growth factor-1, share the feature of triggering nuclear Ca2Â + signals. However, signaling pathways coupling surface receptor activation to nuclear Ca2Â + release, and the phenotypic responses to such signals, differ between agonists. According to earlier hypotheses, the selective control of nuclear Ca2Â + signals by activation of plasma membrane receptors relies on the strategic localization of inositol trisphosphate receptors at the nuclear envelope. There, they mediate Ca2Â + release from perinuclear Ca2Â + stores upon binding of inositol trisphosphate generated in the cytosol, which diffuses into the nucleus. More recently, identification of such receptors at nuclear membranes or perinuclear sarcolemmal invaginations has uncovered novel mechanisms whereby agonists control nuclear Ca2Â + release. In this review, we discuss mechanisms for the selective control of nuclear Ca2Â + signals with special focus on emerging models of agonist receptor activation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 75, October 2014, Pages 40-48
Journal: Journal of Molecular and Cellular Cardiology - Volume 75, October 2014, Pages 40-48
نویسندگان
Cristián Ibarra, Jose Miguel Vicencio, Manuel Varas-Godoy, Enrique Jaimovich, Beverly A. Rothermel, Per Uhlén, Joseph A. Hill, Sergio Lavandero,