Atypical Atm-p53 genetic interaction in osteogenesis is mediated by Smad1 signaling

• 来源期刊: 分子细胞生物学报（英文版）
• 年，卷（期）: 2012,（2）
• 页码范围: 118-120
• 页数: 3页
• 语种: 英文
• DOI: 10.1093/jmcb/mjs006

摘要

Dear Editor, Tumor suppressor p53 is activated in response to genotoxic stress by Atm and other PI3K-like kinases,which phosphorylate p53 and stabilize p53 (Barlow et al.,1997),leading to cell cycle arrest,senescence,or apoptosis (Sherr,1998).As such,p53 and Arm have similar functions in DNA damage response and tumor suppression.Yet recent mouse genetic studies revealed that p53 and Arm play opposite roles in osteogenic differentiation and bone formation,with p53-/- mice showing osteosclerotic phenotypes,whereas Atm -/- mice showing osteoporotic phenotypes (Rasheed et al..2006;Wang et al.,2006).