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色氨酸羟化酶1(Trp1)在与小窝蛋白支架脂质筏结构域相关的信号复合物中的组装。

Assembly of Trp1 in a signaling complex associated with caveolin-scaffolding lipid raft domains.

作者信息

Lockwich T P, Liu X, Singh B B, Jadlowiec J, Weiland S, Ambudkar I S

机构信息

Secretory Physiology Section, Gene Therapy and Therapeutics Branch, NIDCR, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

J Biol Chem. 2000 Apr 21;275(16):11934-42. doi: 10.1074/jbc.275.16.11934.

Abstract

Trp1 has been proposed as a component of the store-operated Ca(2+) entry (SOC) channel. However, neither the molecular mechanism of SOC nor the role of Trp in this process is yet understood. We have examined possible molecular interactions involved in the regulation of SOC and Trp1 and report here for the first time that Trp1 is assembled in signaling complex associated with caveolin-scaffolding lipid raft domains. Endogenous hTrp1 and caveolin-1 were present in low density fractions of Triton X-100-extracted human submandibular gland cell membranes. Depletion of plasma membrane cholesterol increased Triton X-100 solubility of Trp1 and inhibited carbachol-stimulated Ca(2+) signaling. Importantly, thapsigargin stimulated Ca(2+) influx, but not internal Ca(2+) release, and inositol 1,4,5-triphosphate (IP(3))-stimulated I(soc) were also attenuated. Furthermore, both anti-Trp1 and anti-caveolin-1 antibodies co-immunoprecipitated hTrp1, caveolin-1, Galpha(q/11), and IP(3) receptor-type 3 (IP(3)R3). These results demonstrate that caveolar microdomains provide a scaffold for (i) assembly of key Ca(2+) signaling proteins into a complex and (ii) coordination of the molecular interactions leading to the activation of SOC. Importantly, we have shown that Trp1 is also localized in this microdomain where it interacts with one or more components of this complex, including IP(3)R3. This finding is potentially important in elucidating the physiological function of Trp.

摘要

瞬时受体电位通道蛋白1(Trp1)被认为是储存式钙内流(SOC)通道的一个组成部分。然而,目前对于SOC的分子机制以及Trp在这一过程中的作用尚不清楚。我们研究了参与SOC调节和Trp1的可能分子相互作用,并首次在此报告,Trp1组装在与小窝蛋白支架脂筏结构域相关的信号复合物中。内源性人Trp1和小窝蛋白-1存在于经Triton X-100提取的人下颌下腺细胞膜的低密度组分中。质膜胆固醇的消耗增加了Trp1在Triton X-100中的溶解度,并抑制了卡巴胆碱刺激的钙信号传导。重要的是,毒胡萝卜素刺激钙内流,但不刺激细胞内钙释放,并且肌醇1,4,5-三磷酸(IP(3))刺激的I(soc)也减弱。此外,抗Trp1和抗小窝蛋白-1抗体共免疫沉淀了人Trp1、小窝蛋白-1、Gα(q/11)和IP(3)受体3型(IP(3)R3)。这些结果表明,小窝微区为(i)关键钙信号蛋白组装成复合物以及(ii)协调导致SOC激活的分子相互作用提供了一个支架。重要的是,我们已经表明Trp1也定位于这个微区,在那里它与该复合物的一个或多个组分相互作用,包括IP(3)R3。这一发现对于阐明Trp的生理功能可能具有重要意义。

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