کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815453 | 1058475 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Receptor-mediated Ca2Â + and PKC signaling triggers the loss of cortical PKA compartmentalization through the redistribution of gravin
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کلمات کلیدی
ECFPbisindolylmaleimideionomycinβ2ARSOCEEYFPThapsigarginPDE4inositol triphosphatePKCRIIAKAPPLCInsP3AKAP12GPCRpKaSSeCKSCB4eGFP1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid tetrakis(acetoxymethyl ester)sarco/endoplasmic reticulum calcium ATPaseG protein coupled receptor - G پروتئین همراه با پروتئین[Ca2 +]i - [Ca2 +] iAdenosine Triphosphate - آدنوزین تری فسفاتATP - آدنوزین تری فسفات یا ATPSES - آنenhanced cyan fluorescent protein - افزایش پروتئین فلورسنت سیانوژنBAPTA-AM - بیایپیتیای-AMCAM - ساخت به کمک کامپیوترintracellular calcium concentration - غلظت کلسیم داخل سلولیphosphodiesterase type 4 - فسفودی استراز نوع 4phospholipase C - فسفولیپاز CSERCA - قلبBIM - مدلسازی اطلاعات ساختمانStore-operated calcium entry - واردات کلسیم در فروشگاهA-kinase anchoring protein - پروتئین anchoring A-kinaseenhanced yellow fluorescent protein - پروتئین فلورسنت زرد افزایش یافته استenhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استprotein kinase A - پروتئین کیناز AProtein kinase C - پروتئین کیناز سیCalcium - کلسیمGravin - کنتسβ2-adrenergic receptor - گیرنده β2-adrenergicpurinergic receptor - گیرنده پولینیریک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
A-Kinase Anchoring Proteins (AKAPs) direct the flow of cellular information by positioning multiprotein signaling complexes into proximity with effector proteins. However, certain AKAPs are not stationary but can undergo spatiotemporal redistribution in response to stimuli. Gravin, a 300Â kD AKAP that intersects with a diverse signaling array, is localized to the plasma membrane but has been shown to translocate to the cytosol following the elevation of intracellular calcium ([Ca2Â +]i). Despite the potential for gravin redistribution to impact multiple signaling pathways, the dynamics of this event remain poorly understood. In this study, quantitative microscopy of cells expressing gravin-EGFP revealed that Ca2Â + elevation caused the complete translocation of gravin from the cell cortex to the cytosol in as little as 60Â s of treatment with ionomycin or thapsigargin. In addition, receptor mediated signaling was also shown to cause gravin redistribution following ATP treatment, and this event required both [Ca2Â +]i elevation and PKC activation. To understand the mechanism for Ca2Â + mediated gravin dynamics, deletion of calmodulin-binding domains revealed that a fourth putative calmodulin binding domain called CB4 (a.a. 670-694) is critical for targeting gravin to the cell cortex despite its location downstream of gravin's membrane-targeting domains, which include an N-terminal myristoylation site and three polybasic domains. Finally, confocal microscopy of cells co-transfected with gravin-EYFP and PKA RII-ECFP revealed that gravin redistribution mediated by ionomycin, thapsigargin, and ATP each triggered the gravin-dependent loss of PKA localized at the cell cortex. Our results support the hypothesis that gravin redistribution regulates cross-talk between PKA-dependent signaling and receptor-mediated events involving Ca2Â + and PKC.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 25, Issue 11, November 2013, Pages 2125-2135
Journal: Cellular Signalling - Volume 25, Issue 11, November 2013, Pages 2125-2135
نویسندگان
Micah B. Schott, Bryon Grove,