期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 408, 期 2, 页码 214-217出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2011.03.112
关键词
Inositol 1,4,5-trisphosphate receptor; KRAS-induced actin-interacting protein; Calcium release; Calcium signaling
资金
- Ministry of Education, Culture, Sports, Science, and Technology
- Japan Society for the Promotion of the Science
- Clinical Research Foundation
- Sumitomo Foundation
- Grants-in-Aid for Scientific Research [21390102] Funding Source: KAKEN
KRAS-induced actin-interacting protein (KRAP) was originally characterized as a filamentous- actin-interacting protein. We have recently found that KRAP is an associated molecule with inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) and is responsible for the proper subcellular localization of IP3R. Since it remains unknown whether KRAP regulates the IP3R-mediated Ca2+ signaling, we herein examined the effects of KRAP on the IP3R-mediated Ca2+ release by Ca2+ imagings in the cultured HEK293 or MCF7 cells. Reduction of KRAP protein by KRAP-specific siRNA diminishes ATP-induced Ca2+ release and the ATP-induced Ca2+ release is completely quenched by the pretreatment with the IP3R inhibitor but not with the ryanodine receptor inhibitor, indicating that KRAP regulates IP3R-mediated Ca2+ release. To further reveal mechanistic insights into the regulation of IP3R-mediated Ca2+ release by KRAP, we examined the effects of the KRAP-knockdown on the releasable Ca2+ content of intracellular Ca2+ stores. Consequently, reduction of KRAP does not affect the amount of ionophore- or Ca2+-ATPase inhibitor-induced Ca2+ release in the HEK293 cells, indicating that releasable Ca2+ content of intracellular Ca2+ stores is not altered by KRAP. Thus, KRAP is involved in the proper regulation of IP3R-mediated Ca2+ release. (C) 2011 Elsevier Inc. All rights reserved.
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