Academic Journal
Ca2+ influx and protein scaffolding via TRPC3 sustain PKC{beta} and ERK activation in B cells
| العنوان: | Ca2+ influx and protein scaffolding via TRPC3 sustain PKC{beta} and ERK activation in B cells |
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| المؤلفون: | Numaga, Takuro, Nishida, Motohiro, Kiyonaka, Shigeki, Kato, Kenta, Katano, Masahiro, Mori, Emiko, Kurosaki, Tomohiro, Inoue, Ryuji, Hikida, Masaki, Putney, James W., Mori, Yasuo |
| بيانات النشر: | Company of Biologists |
| سنة النشر: | 2010 |
| المجموعة: | HighWire Press (Stanford University) |
| مصطلحات موضوعية: | RESEARCH ARTICLE |
| الوصف: | Ca2+ signaling mediated by phospholipase C that produces inositol 1,4,5-trisphosphate [Ins(1,4,5 P 3 ] and diacylglycerol (DAG controls lymphocyte activation. In contrast to store-operated Ca2+ entry activated by Ins(1,4,5 P 3 -induced Ca2+ release from endoplasmic reticulum, the importance of DAG-activated Ca2+ entry remains elusive. Here, we describe the physiological role of DAG-activated Ca2+ entry channels in B-cell receptor (BCR signaling. In avian DT40 B cells, deficiency of transient receptor potential TRPC3 at the plasma membrane (PM impaired DAG-activated cation currents and, upon BCR stimulation, the sustained translocation to the PM of protein kinase Cβ (PKCβ that activated extracellular signal-regulated kinase (ERK. Notably, TRPC3 showed direct association with PKCβ that maintained localization of PKCβ at the PM. Thus, TRPC3 functions as both a Ca2+-permeable channel and a protein scaffold at the PM for downstream PKCβ activation in B cells. |
| نوع الوثيقة: | text |
| وصف الملف: | text/html |
| اللغة: | English |
| Relation: | http://jcs.biologists.org/cgi/content/short/jcs.061051v1; http://dx.doi.org/10.1242/jcs.061051 |
| DOI: | 10.1242/jcs.061051 |
| الاتاحة: | http://jcs.biologists.org/cgi/content/short/jcs.061051v1 https://doi.org/10.1242/jcs.061051 |
| Rights: | Copyright (C) 2010, Company of Biologists |
| رقم الانضمام: | edsbas.BD5BEAF5 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1242/jcs.061051 |
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