کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10816342 | 1058564 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Roles of protein kinase C in regulation of P2X7 receptor-mediated calcium signalling of cultured type-2 astrocyte cell line, RBA-2
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کلمات کلیدی
BzATPPKCphorbol 12-myristate 13 acetateCa2+ - Ca2 +PMA - LDC ها[Ca2+]i - [Ca2 +] iadenosine 5′-triphosphate - آدنوزین 5'-تری فسفاتATP - آدنوزین تری فسفات یا ATPAstrocytes - آستروسیتCalcium signalling - سیگنالینگ کلسیمintracellular calcium concentration - غلظت کلسیم داخل سلولیProtein kinase C - پروتئین کیناز سیCalcium - کلسیمP2X7 receptor - گیرنده P2X7
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
The role of protein kinase C (PKC) on regulation of P2X7 receptor-mediated Ca2+ signalling was examined on RBA-2 astrocytes. Activation of PKC decreased the receptor-mediated Ca2+ signalling and the decrease was restored by PKC inhibitors. Down regulation of PKC also caused a decrease in the Ca2+ signalling. Thus PKC might play a dual role on the P2X7 receptor signalling. Successive stimulation of the P2X7 receptor induced a gradual decline of Ca2+ signalling but PKC inhibitors failed to restore the decline. Nevertheless, PMA stimulated translocation of PKC-α, -βI, -βII, and -γ, but only anti-PKC-γ co-immunoprecipitated the receptors. To examine the role of PKC-γ, Ca2+ signalling was measured by Ca2+ imaging. Our results revealed that the agonist-stimulated Ca2+ signalling were reduced in the cells that the transfection of either P2X7 receptor or PKC-γ morpholino antisense oligo was identified. Thus, we concluded that PKC-γ interacted with P2X7 receptor complex and positively regulated the receptor-mediated Ca2+ signalling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 17, Issue 11, November 2005, Pages 1384-1396
Journal: Cellular Signalling - Volume 17, Issue 11, November 2005, Pages 1384-1396
نویسندگان
Amos C. Hung, You-Jing Chu, Ya-Hui Lin, Ju-Yun Weng, Hammer B. Chen, Yin-Chung Au, Synthia H. Sun,