StudyofintracellularlocalizationofIP3-receptortype2

IP3受体2型细胞内定位的研究

• 批准号: 22592072
• 负责人: MASUDA Wataru
• 金额: $ 2.91万
• 依托单位: Kyushu Dental College
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22592072/
• 关键词: IP3 受容体; IRAG; 細胞内局在; IP3受容体; 唾液腺; IP_3受容体type2

IP3R type I (IP3R-I) was phosphorylated by PKA and this causesthe potentiation of carbachol (CCh)-induced Ca-release from IP3R-I. In the presence ofIRAG and PKG Iβ, IP3R-I forms a complex with these molecules and this causes theloss of both the phosphorylation by PKA and the potentiation of CCh-inducedCa-release. IP3R type II (IP3R-II) also be able to form a complex with IRAG and PKG Iβ. However, the phosphorylation of IP3R-II by PKA and the potentiation of carbachol(CCh)-induced Ca-release from IP3R-II were not inhibited by forming a complex. Inthis study, we identified the regions of IP3R molecules, which were required forinteraction with IRAG. In the IP3R-I, the region was much close to the phosphorylationsite, while it was far from the phosphorylation site in the IP3R-II. This result indicatedthat the interaction of IP3R-I with IRAG spatially did not permit PKA to access tophosphorylation site.

IP 3R-I可被PKA磷酸化，从而增强卡巴胆碱（CCh）诱导的IP 3R-I释放钙的能力。在IRAG和PKG Iβ存在下，IP 3R-I与这些分子形成复合物，这导致PKA磷酸化的丧失和CCh诱导的Ca-2+释放的增强。II型IP 3R（IP 3R-II）也能与IRAG和PKG Iβ形成复合物。然而，磷酸化的IP 3R-II的PKA和增强卡巴胆碱（CCh）诱导的Ca-释放IP 3R-II不抑制形成复合物。在这项研究中，我们确定了IP 3R分子与IRAG相互作用所需的区域。在IP 3R-I中，该区域更靠近磷酸化位点，而在IP 3R-II中，该区域远离磷酸化位点。这一结果表明IP 3R-I与IRAG的相互作用在空间上不允许PKA进入磷酸化位点。

项目成果

IP3R /IRAG/PKG Iβ複合体におけるCa2+放出機構

IP3R/IRAG/PKG Iβ 复合物中的 Ca2+ 释放机制

• 发表时间: 2010
• 作者: 増田渉;Betzenhauser M.J.;Yule D.I.
• 通讯作者: Yule D.I.