Background

JNK is also named as MAPK8 (Mitogen-activated protein kinase 8), PRKM8, SAPK1, SAPK1C and belongs to the MAP kinase subfamily. JNK is activated by dual phosphorylation at a Thr-Pro-Tyr motif during response to UV light. JNK functions to phosphorylate c-Jun at N-terminal serine regulatory sites of Ser-63 and Ser-73, mapping within the transactivation domain. Phosphorylation of these sites in response to UV results in transcriptional activation of c-Jun. JNK activity is abnormally elevated in obesity. Furthermore, an absence of JNK results in decreased adiposity, significantly improved insulin sensitivity, and enhanced insulin receptor signaling capacity in 2 different models of mouse obesity, including ob/ob. JNK is a crucial mediator of obesity and insulin resistance and a potential target for therapeutics. The ELISA kit is suitable for testing cell lysates.