کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815310 | 1058467 | 2014 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Does GRK-β arrestin machinery work as a “switch on” for GPR17-mediated activation of intracellular signaling pathways?
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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![عکس صفحه اول مقاله: Does GRK-β arrestin machinery work as a “switch on” for GPR17-mediated activation of intracellular signaling pathways? Does GRK-β arrestin machinery work as a “switch on” for GPR17-mediated activation of intracellular signaling pathways?](/preview/png/10815310.png)
چکیده انگلیسی
On the other hand, purinergic ligand exclusively recruited the GRK5 subtype, and induced, via a G protein-independent/β-arrestin-dependent mechanism, a receptor/β-arrestin stable association, slower and sustained ERK stimulation and marginal CREB activation. These results show that purinergic and cysLT ligands, through the recruitment of specific GRK isoforms, address distinct intracellular pathways, most likely reinforcing the same final response. The identification of these mechanisms and players controlling GPR17 responses during OPC differentiation could be useful to identify new targets in demyelination diseases and to develop new therapeutical strategies.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 26, Issue 6, June 2014, Pages 1310-1325
Journal: Cellular Signalling - Volume 26, Issue 6, June 2014, Pages 1310-1325
نویسندگان
Simona Daniele, Maria Letizia Trincavelli, Marta Fumagalli, Elisa Zappelli, Davide Lecca, Elisabetta Bonfanti, Pietro Campiglia, Maria P. Abbracchio, Claudia Martini,