Analysis of the regulatory mechanisms of G protein-coupled receptor signaling

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293013
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Nara Institute of Science and Technology
• Principal Investigator: Itoh Hiroshi 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (10183005)
• Co-Investigator(Kenkyū-buntansha): KOBAYASHI Tetsuo 奈良先端科学技術大学院大学, バイオサイエンス研究科, 助教 (80433994)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: Gタンパク質 / GPCR

Outline of Final Research Achievements

We generated agonistic monoclonal antibodies against GPR56 and showed that the antibodies inhibit the migration of human glioma cells through Gq, Rho, and Rho kinase pathway. We found the possibility that GPR56 transmembrane region and latrophilin1 extracellular region forms a chimera receptor in GABAegic neurons, and latrotoxin, a latrophilin1 ligand, induces cell response mediated by the chimera receptor. We demonstrated that Ric-8 functions as a positive regulator for GPCR signaling system by regulating two post-translational modifications, ubiquitination and palmitoylation, on G proteins.

Free Research Field

細胞生物学