JNK: a new therapeutic target for diabetes.
Jun N-terminal kinase (JNK) regulates the transcription factor AP-1, which is implicated in the controlled expression of many genes involved in the immune response. For this reason, drug discovery efforts have focused on the development of JNK inhibitors for chronic inflammatory diseases. However, recent genetic evidence and emerging pharmacological data indicate that activated JNK could be critical in causing diabetes, insulin resistance and obesity. Indeed, if JNK is considered as a stress-activated protein kinase, there appear to be multiple mechanisms through which it might promote diabetes.
Bennett
Brydon L
BL
Celgene Corporation, 4550 Towne Centre Court, San Diego, CA 92121, USA. bbennett@celgene.com
Satoh
Yoshitaka
Y
Lewis
Alan J
AJ
D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D016503:Drug Delivery Systems; D004789:Enzyme Activation; D006801:Humans; D007333:Insulin Resistance; D048031:JNK Mitogen-Activated Protein Kinases; D048670:MAP Kinase Kinase 4; D051379:Mice; D020929:Mitogen-Activated Protein Kinase Kinases / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D010179:Pancreas / Q000276:immunology / Q000378:metabolism; D011972:Receptor, Insulin / Q000502:physiology; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D014409:Tumor Necrosis Factor-alpha; D011972:Receptor, Insulin; D048031:JNK Mitogen-Activated Protein Kinases; D048670:MAP Kinase Kinase 4; D020929:Mitogen-Activated Protein Kinase Kinases