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.

I 型 IP3R (IP3R-I) 被 PKA 磷酸化，这会增强卡巴胆碱 (CCh) 诱导的 IP3R-I 的 Ca 释放。在 IRAG 和 PKG Iβ 存在的情况下，IP3R-I 与这些分子形成复合物。导致 PKA 磷酸化的丧失和 CCh 诱导的 IP3R II 型 (IP3R-II) 钙释放的增强也能够形成复合物。然而，PKA 对 IP3R-II 的磷酸化和卡巴胆碱 (CCh) 诱导的 IP3R-II 钙释放的增强并未因形成复合物而受到抑制。与IRAG相互作用所需的分子，在IP3R-I中，该区域距离磷酸化位点很近，而在IP3R-I中则远离磷酸化位点。 IP3R-II。该结果表明IP3R-I与IRAG在空间上的相互作用不允许PKA到达磷酸化位点。

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.