2016 Fiscal Year Final Research Report
fundamental Study on the mechanism of GPCR trafficking to cell surface
| Project/Area Number |
26460061
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Biological pharmacy
|
|---|
| Research Institution | Okayama University of Science |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Keywords | G蛋白質共役型受容体蛋白質共役型受容体 / ロイコトリエンB4 / リン酸化 / BLT1 |
|---|
| Outline of Final Research Achievements |
BLT1 is expressed in phagocytic and immune cells and plays crucial roles in various inflammatory diseases. Although BLT1 is phosphorylated upon stimulation with LTB4, precise functions of this modification remain elusive. We determined all phosphorylated sites, basal and ligand-induced modification residues of BLT1. The ligand-induced phosphorylations occurred at different concentration of LTB4, and each modification facilitated basal phosphorylations. Because the concentration of LTB4 exposed to BLT1 on leukocytes is raised gradually during migration toward inflammatory sites, the degree of phosphorylations could be enhanced in parallel with increase in LTB4. At high LTB4, deficiencies in the phosphorylations impaired chemotaxis and degranulation in BLT1 expressing cells. These results suggest that the phosphorylations of BLT1 recognize a rise in LTB4, resulting in the precise migration toward inflammatory regions and initiation of local responses, e.g., degranulation.
|
| Free Research Field |
生化学、分子生物学
|
