Abl1 deletion in gut stem cells suppresses p53 induction and promotes colitis-associated tumor formation

• 来源期刊: 分子细胞生物学报（英文版）
• 年，卷（期）: 2020,（9）
• 所属期刊栏目: Letters to the Editor
• 页码范围: 738-740
• 页数: 3页
• 语种: 英文
• DOI: 10.1093/jmcb/mjaa022

摘要

Dear Editor, Abl1,when fused with BCR,expresses fusion protein BCR-ABL that underlies the etiology of chronic myeloid leukemia and is therapeutically targeted by Imatinib Mesylate (Khatri et al.,2016).However,the function of proto-oncogene product Abl1 remains not fully under-stood.This non-receptor tyrosine kinase can be activated by growth factors,DNA damage,oxidative stress,and microbial pathogens (Wang,2014).