作者: Basant Kumar Thakur , Tino Dittrich , Prakash Chandra , Annette Becker , Yannick Lippka
DOI: 10.1016/J.BBRC.2012.06.075
关键词:
摘要: Inactivation of p53 protein by endogenous and exogenous carcinogens is involved in the pathogenesis different human malignancies. In cancer associated with SV-40 DNA tumor virus, considered to be non-functional mainly due its interaction large T-antigen. Using 293T cell line (HEK293 cells transformed T antigen) as a model, we provide evidence that one critical downstream targets FK866-mediated killing cells. A reduced rate apoptosis an increased number S-phase was accompanied after knockdown these Inhibition NAMPT FK866, or inhibition SIRT nicotinamide decreased proliferation triggered death involving acetylation pathway. Additionally, attenuated effect FK866 on proliferation, apoptosis, cycle arrest. The data presented here shed light two important facts: (1) active presence inhibitor pathway; (2) induced at Lys382, which required for functional activity p53.