A nonsense mutation of Stim1 identified in stroke-prone spontaneously hypertensive rats decreased the store-operated calcium entry in astrocytes.

In this study, we evaluated activity of the store-operated Ca(2+)-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 Ca(2+) signaling regulated by SOCE and that the impaired SOCE activity might be responsible for pathological phenotypes in SHRSP.
PMID: 27237974 [PubMed - as supplied by publisher]

Source: Biochemical and Biophysical Research communications - May 25, 2016 Category: Biochemistry Authors: Ohara H, Nabika T Tags: Biochem Biophys Res Commun Source Type: research