2012 Fiscal Year Final Research Report
StudyofintracellularlocalizationofIP3-receptortype2
| Project/Area Number |
22592072
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Functional basic dentistry
|
|---|
| Research Institution | Kyushu Dental College |
|---|
Principal Investigator |
MASUDA Wataru 九州歯科大学, 歯学部, 助教 (80295865)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
JIMI Eijirou 九州歯科大学, 歯学部, 教授 (40276598)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
FUKUSHIMA Hidefumi 九州歯科大学, 歯学部, 講師 (70412624)
|
|---|
| Research Collaborator |
D.I. Yule 米国ロチェスター大学, 教授
|
|---|
| Project Period (FY) |
2010 – 2012
|
| Keywords | IP3 受容体 / IRAG / 細胞内局在 |
|---|
| Research Abstract |
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.
|
