The role of JNK proteins in metabolism.
The stress-activated c-Jun amino-terminal kinase (JNK) plays a pivotal role in metabolic conditions such as obesity, insulin resistance, and type 2 diabetes. Intricate tissue-specific tweaking of JNK activity in preclinical models of metabolic diseases reveals a complex interplay among local and systemic effects on carbohydrate and lipid metabolism. Synthesis of these entangled effects illustrates that for JNK inhibitors to have therapeutic impact, they must function in multiple cell types to modulate JNK activity.
Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Sara N
SN
Vallerie
Gökhan S
GS
Hotamisligil
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001854:Bone Marrow Cells / Q000378:metabolism; D002490:Central Nervous System / Q000378:metabolism; D004734:Energy Metabolism; D006801:Humans; D050417:Insulin-Secreting Cells / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008659:Metabolic Diseases / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D013312:Stress, Physiological
D048031:JNK Mitogen-Activated Protein Kinases