| Literature DB >> 17689489 |
Yoichiro Takahashi1, Hiroyuki Watanabe, Manabu Murakami, Kyoichi Ono, Yoshiko Munehisa, Takashi Koyama, Kiyoshi Nobori, Toshihiko Iijima, Hiroshi Ito.
Abstract
We investigated the functional role of STIM1, a Ca(2+) sensor in the endoplasmic reticulum (ER) that regulates store-operated Ca(2+) entry (SOCE), in vascular smooth muscle cells (VSMCs). STIM1 was mainly localized at the ER and plasma membrane. The knockdown of STIM1 expression by small interfering (si) RNA drastically decreased SOCE. In contrast, an EF-hand mutant of STIM1, STIM1(E87A), produced a marked increase in SOCE, which was abolished by co-transfection with siRNA to transient receptor potential canonical 1 (TRPC1). In addition, transfection with siRNA against STIM1 suppressed phosphorylation of cAMP-responsive element binding protein (CREB) and cell growth. These results suggest that STIM1 is an essential component of SOCE and that it is involved in VSMC proliferation.Entities:
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Year: 2007 PMID： 17689489 DOI： 10.1016/j.bbrc.2007.07.096
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575