【摘 要】
：
The depletion of Ca2+ from the endoplasmic reticulum (ER) stores, by the stimulation of immune cells, triggers the influx of Ca2+ through store-operated Ca2+ re
【机 构】
：
SherAli,InstituteofBiophysics,CAS,Beijing,China
【出 处】
：
The 9th Asian Biophysics Association Symposium (ABA2015)(第九届
论文部分内容阅读
The depletion of Ca2+ from the endoplasmic reticulum (ER) stores, by the stimulation of immune cells, triggers the influx of Ca2+ through store-operated Ca2+ release-activated Ca2+ (CRAC) channels, thereby, elicit an important signal for the activation and proliferation of lymphocytes.CRAC channel works by the physical interaction of STIM1 (ER Ca2+ sensor) and pore forming subunit, Orai1.2-aminoethyldiphenyl borate (2APB), an IP3 receptor antagonist, elicits both potentiating and inhibiting effect on Ca2+ influx via CRAC channels.In this study we focused on understanding the mechanism of its potentiation effect.We identified some of the key residues which are located in the extracellular region of the pore, plays a vital role in the potentiating effect caused by 2APB.Mutation of such residues completely eliminate the potentiating effect.Furthermore, that mutant with small side chain such as C, A, G barely could or totally counldnt generate 2-APB induced potentiation current while mutation with large side chain such as M and I could generate 2-APB induced potentiation current as WT.It is already known that, this extracellular region of the pore is involve in the gating of the channel and hence our results demonstrates that gating and the potentiating effect caused by 2APB might be closely coupled together.
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