کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815828 | 1058505 | 2011 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A role for protein kinase C in the regulation of membrane fluidity and Ca2+ flux at the endoplasmic reticulum and plasma membranes of HEK293 and Jurkat cells
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: A role for protein kinase C in the regulation of membrane fluidity and Ca2+ flux at the endoplasmic reticulum and plasma membranes of HEK293 and Jurkat cells A role for protein kinase C in the regulation of membrane fluidity and Ca2+ flux at the endoplasmic reticulum and plasma membranes of HEK293 and Jurkat cells](/preview/png/10815828.png)
چکیده انگلیسی
Protein kinase C (PKC) plays a prominent role in the regulation of a variety of cellular functions, including Ca2+ signalling. In HEK293 and Jurkat cells, the Ca2+ release and Ca2+ uptake stimulated by several different activators were attenuated by activation of PKC with phorbol myristate acetate (PMA) or 1-oleoyl-2-acetyl-sn-glycerol (OAG) and potentiated by PKC inhibition with Gö6983 or knockdown of PKCα or PKCβ using shRNA. Immunostaining and Western blotting analyses revealed that PKCα and PKCβII accumulated at the plasma membrane (PM) and that these isoforms, along with PKCβI, also translocated to the endoplasmic reticulum (ER) upon activation with PMA. Measurements of membrane fluidity showed that, like the cell membrane stabilizers bovine serum albumin (BSA) and ursodeoxycholate (UDCA), PMA and OAG significantly reduced the fluidity of both the PM and ER membranes; these effects were blocked in PKC-knockdown cells. Interestingly, both BSA and UDCA inhibited the Ca2+ responses to agonists to the same extent as PMA, whereas Tween 20, which increases membrane fluidity, raised the internal Ca2+ concentration. Thus, activation of PKC induces both translocation of PKC to the PM and ER membranes and downregulation of membrane fluidity, thereby negatively modulating Ca2+ flux.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 23, Issue 2, February 2011, Pages 497-505
Journal: Cellular Signalling - Volume 23, Issue 2, February 2011, Pages 497-505
نویسندگان
Lihong Chen, Qingli Meng, Xian Jing, Pingxiang Xu, Dali Luo,