| General information | Literature | Expression | lncRNA |Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 5563 |
Name | PRKAA2 |
Sentence | From PubMed database |
| AMPKalpha2 reduces renal epithelial transdifferentiation and inflammation after injury through interaction with CK2beta. | TGFbeta1/Smad, Wnt/beta-catenin and snail1 are preferentially activated in renal tubular epithelia after injury, leading to epithelial-mesenchymal transition (EMT). The stress response is coupled to EMT and kidney injury; however, the underlying mechanism of the stress response in EMT remains elusive. AMP-activated protein kinase (AMPK) signalling is responsive to stress and regulates cell energy balance and differentiation. We found that knockdown of AMPKalpha, especially AMPKalpha2, enhanced EMT by up-regulating beta-catenin and Smad3 in vitro. AMPKalpha2 deficiency enhanced EMT and fibrosis in a murine unilateral ureteral obstruction (UUO) model. AMPKalpha2 deficiency also increased the expression of chemokines KC and MCP-1, along with enhanced infiltration of inflammatory cells into the kidney after UUO. CK2beta interacted physically with AMPKalpha and enhanced AMPKalpha Thr172 phosphorylation and its catalytic activity. Thus, activated AMPKalpha signalling suppresses EMT and secretion of chemokines in renal tubular epithelia through interaction with CK2beta to attenuate renal injury.CI - Copyright (c) 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |