| Literature DB >> 22183808 |
Congyan Pan1, Ji Zheng, Yanyun Wu, Yingxiao Chen, Likun Wang, Zhansong Zhou, Wenxuan Yin, Guangju Ji.
Abstract
Previous studies have indicated that ERp44 inhibits inositol 1,4,5-trisphosphate (IP(3))-induced Ca(2+) release (IICR) via IP(3)R(1), but the mechanism remains largely unexplored. Using extracellular ATP to induce intracellular calcium transient as an IICR model, Ca(2+) image, pull down assay, and Western blotting experiments were carried out in the present study. We found that extracellular ATP induced calcium transient via IP(3)Rs (IICR) and the IICR were markedly decreased in ERp44 overexpressed Hela cells. The inhibitory effect of C160S/C212S but not C29S/T396A/ΔT(331-377) mutants of ERp44 on IICR were significantly decreased compared with ERp44. However, the binding capacity of ERp44 to L3V domain of IP(3)R(1) (1L3V) was enhanced by ERp44 C160S/C212S mutation. Taken together, these results suggest that the mutants of ERp44, C160/C212, can more tightly bind to IP(3)R(1) but exhibit a weak inhibition of IP(3)R(1) channel activity in Hela cells.Entities:
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Year: 2011 PMID： 22183808 PMCID： PMC4875245 DOI： 10.1007/s13238-011-1116-0
Source DB: PubMed Journal: Protein Cell ISSN： 1674-800X Impact factor: 14.870