SRP493421 PRJNA1083895 GSE260876 TAX1BP1 deficiency impair initiation of autophagic flow in HK-2 cells through downregulate AMPK-ULK1 pathway Selective autophagy receptor can combine with substrate in cells to degrade them and maintain cellular homeostasis. TAX1BP1, a kind of selective autophagy receptor, has N-terminal SKIP carboxyl homology (SKICH) domain (LC3-Interacting Region) and a C-terminal ubiquitin binding domain (UBD).TAX1BP1 can also be a potential regulatory factor to influence macroautophagy initiation. In order to research the function of TAX1BP1in renal tubular epithelial cells, we knockout and over expressive TAX1BP1 in HK-2 cells and research the state of autophagy flow and senescence. We found that TAX1BP1 knockout could impair initiation of autophagic flow, causing obstruction in LC3 lipidation. Farther, TAX1BP1 knockout could bring senescence and sensitivity in damage factor. Overall design: Bulk RNA-seq between WT HK-2 cells and TAX1BP1-KO HK-2 cells, each group has three biological duplication GSE260876