期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 476, 期 4, 页码 406-411出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.05.134
关键词
Stromal interaction molecule-1; Stroke-prone spontaneously hypertensive rat; Store-operated Ca2+-entry
资金
- JSPS KAKENHI [23890115, 24790846]
- Grants-in-Aid for Scientific Research [26290067, 24790846, 23890115] Funding Source: KAKEN
We previously identified a nonsense mutation in the stromal interaction molecule-1 (Stim1) resulting in expression of a truncated STIM1 in the stroke-prone spontaneously hypertensive rat (SHRSP). In this study, we evaluated activity of the store -operated Ca2+-entry (SOCE) regulated by STIM1 to clarify putative functional abnormalities of the truncated STIM1. As a result, reduced SOCE activity resulting in suppression of cyclooxygenase-2 expression induced by SOCE was found in cultured astrocytes with the truncated STIM1 when compared with those with the wild-type. Our results indicated that the truncated STIM1 impaired Ca2+ signaling regulated by SOCE and that the impaired SOCE activity might be responsible for pathological phenotypes in SHRSP. (C) 2016 Elsevier Inc. All rights reserved.
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