Analysis of novel oxidative stress response mechanism via ribosome

2017 Fiscal Year Final Research Report

• Project/Area Number: 25293064
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: General medical chemistry
• Research Institution: Hirosaki University
• Principal Investigator: Itoh Ken 弘前大学, 医学研究科, 教授 (10323289)
• Co-Investigator(Kenkyū-buntansha): 松宮 朋穂 弘前大学, 医学研究科, 助教 (30344592)
• Co-Investigator(Renkei-kenkyūsha): MIMURA Junsei 弘前大学, 大学院医学研究科, 講師 (60344884) ; MARUYAMA Atsushi 東北医科薬科大学, 薬学部, 講師 (10431438) ; HIMENO Hyouta 弘前大学, 農学生命科学部, 教授 (80208785)
• Project Period (FY): 2013-04-01 – 2018-03-31
• Keywords: リボソーム / アミノ酸飢餓 / GCN1L1 / Nrf2

Outline of Final Research Achievements

In order to clarify the roles of GCN1L1, we generated GCN1L1 mice lacking RWDBD (GCN1L1 delta RWDBD) that is required for GCN1L1 binding to RWD possessing proteins such as GCN2 and DFRP2. The embryos of GCN1L1 delta RWDBD mice shows growth retardation starting from at least 12.5 dpc and died soon after birth. The embryonic fibroblasts obtained from GCN1L1 delta RWDBD mice shows slower prolifferation compared to those of wild-type mice associting with G2/M cell cycle arrest and decreased levels of DRG2 that heterodimerizes with DFRP2. These results suggest that GCN1L1 controls cell proliferation via the regulation of DRG2/DFRP2.

Free Research Field

分子生物学