Regulation of neuronal physiology by Ca2+ release through the IP3R

被引:7
作者
Hasan, Gaiti [1 ]
Sharma, Anamika [1 ]
机构
[1] Natl Ctr Biol Sci, Tata Inst Fundamental Res, Bellary Rd, Bengaluru 560080, India
关键词
INOSITOL; ITPR1; DELETION; RECEPTORS; MUTATION; ATAXIA; ENTRY; ORAI;
D O I
10.1016/j.cophys.2020.06.001
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Identification of mutations in the gene encoding the inositol 1,4,5-trisphosphate receptor Type 1 (IP(3)R1) as causative for Spinocerebellar Ataxia 15, 29 and Gillespie Syndrome emphasize the importance of understanding how the IP3R impacts neuronal function and physiology. Here we discuss how cellular changes due to IP3 mediated Ca2+ release affect systemic physiology in Drosophila and mouse. The relevance of these findings to recently identified human neurological conditions are also discussed.
引用
收藏
页码:1 / 8
页数:8
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