纤维化
衰老
炎症体
肺纤维化
癌症研究
A549电池
基因剔除小鼠
炎症
内分泌学
内科学
生物
细胞生物学
化学
医学
肺
受体
作者
Xin Gu,Haoyu Meng,Chengyi Peng,Shiyu Lin,Baihong Li,Lin Zhao,Yang Xue,Guangyan Wang,Wenyuan Cai,Jiawen Zhou,Shuiyuan Liu,Peng Wu,Yingqiang Du,Jianliang Jin,Xiaoyan Wang
摘要
P16 accumulation promoted activation of integrin- inflammasome pathway and cell glycolysis by binding to the N- terminal of SGK1, intefering with the interaction between the E3 ubiquitin ligase NEDD4L and SGK1, thereby inhibiting K48- polyubiquitin- dependent degradation of SGK1 mediated by the NEDD4L-Ubch5 complex. ABT263 or EMD638683 could be used as potential drugs to treat pulmonary fibrosis in obese patients.
科研通智能强力驱动
Strongly Powered by AbleSci AI