Background/Aims: The c-Jun amino-terminal kinase (JNK) signaling pathway is activated in human kidney diseases and promotes renal injury in experimental glomerulonephritis. In this study, we ex
The JNK pathway modulates AP-1 activity. While in some cells it may have proliferative and protective roles, in neuronal cells it is involved in apoptosis in response to stress or withdrawal of surviv
The file contains raw data related to the article "JNK signaling activation in the Ube3a maternal deficient mouse model", available from https://www.sciencedirect.com/science/article/pii/S096999612030
