CALRETICULIN INHIBITS REPETITIVE INTRACELLULAR CA2+ WAVES
CALRETICULIN INHIBITS REPETITIVE INTRACELLULAR CA2+ WAVES
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DOI：
10.1016/0092-8674(95)90473-5
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发表时间：
1995-09-08
期刊：
影响因子：
64.5
通讯作者：
LECHLEITER, JD
中科院分区：
文献类型：
--
作者：
CAMACHO, P;LECHLEITER, JD
肌醇1,4,5-三磷酸（IP3）介导的钙（Ca2+）信号传导受细胞质和腔内调节机制的影响。在爪蟾卵母细胞中，IP3受体（IP(3)R）的Ca2+敏感门控产生Ca2+释放的重复波。我们通过使用Ca2+波活性作为敏感的Ca2+释放测定，研究了腔内Ca2+结合蛋白钙网蛋白（CRT）在ip3介导的Ca2+信号传导中的作用。过表达CRT抑制ip3诱导的重复Ca2+波。缺失突变表明，CRT抑制是由高亲和力-低容量Ca2+结合域介导的，这对Ca2+存储贡献不大。CRT在细胞内Ca2+信号传导中的这种新功能可能受到Ca2+占据高亲和力结合位点的调节。
Inositol 1,4,5-trisphosphate (IP3)-mediated calcium (Ca2+) signaling is subject to cytosolic and luminal regulatory mechanisms. In Xenopus oocytes, Ca2+-sensitive gating of the IP3 receptor (IP(3)R) produces repetitive waves of Ca2+ release. We examined the role of the luminal Ca2+-binding protein calreticulin (CRT) in IP3-mediated Ca2+ signaling by using Ca2+ wave activity as a sensitive Ca2+ release assay. Overexpression of CRT inhibited repetitive IP3-induced Ca2+ waves. Deletion mutagenesis demonstrated that CRT inhibition was mediated by the high affinity-low capacity Ca2+-binding domain, which contributes little to Ca2+ storage. This novel function of CRT in intracellular Ca2+ signaling may be regulated by Ca2+ occupancy of the high affinity binding site.