Molecular bases and the counteracting strategy for the detrimental phenotype of Max-null ES cells

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670147
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: General medical chemistry
• Research Institution: Saitama Medical University
• Principal Investigator: OKUDA Akihiko 埼玉医科大学, 医学部, 教授 (60201993)
• Co-Investigator(Kenkyū-buntansha): KATANO Miyuki 埼玉医科大学, 医学部, 助手 (60521060)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: ES細胞 / 癌細胞 / アポトーシス / c-Myc / Nanog

Outline of Final Research Achievements

We have previously demonstrated that homozygous knockout of Max gene encoding indispensable partner protein for MYC family protein in ES cells leads to loss of pluripotent properties and extensive cell death. Furthermore, we have also demonstrated that such detrimental phenotypes of Max-null ES cells can be eased by the forced expression of Nanog encoding one of pluripotency marker proteins. In this research project, we have uncovered a part of the molecular mechanisms underscoring the phenotypes associated with ablation of Max expression in ES cells and the rescue effect attained by Nanog overexpression on Max-null ES cells.

Free Research Field

幹細胞生物s学