Description
Protocol
Available protocols: ELISA+
Specificity / Sensitivity
PathScan
Species Reactivity: Human, Mouse
Background
The stress-activated protein kinase/Jun-amino-terminal kinase SAPK/JNK is potently and preferentially activated by a variety of environmental stresses, including UV and gamma radiation, ceramides, inflammatory cytokines, and in some instances, growth factors and GPCR agonists (1-6). As with the other MAPKs, the core signaling unit is composed of a MAPKKK, typically MEKK1-MEKK4, or by one of the mixed lineage kinases (MLKs), which phosphorylate and activate MKK4/7. Upon activation, MKKs phosphorylate and activate the SAPK/JNK kinase (2). Stress signals are delivered to this cascade by small GTPases of the Rho family (Rac, Rho, cdc42) (3). Both Rac1 and cdc42 mediate the stimulation of MEKKs and MLKs (3). Alternatively, MKK4/7 can be activated in a GTPase-independent mechanism via stimulation of a germinal center kinase (GCK) family member (4). There are three SAPK/JNK genes each of which undergoes alternative splicing, resulting in numerous isoforms (3). SAPK/JNK, when active as a dimer, can translocate to the nucleus and regulate transcription through its effects on c-Jun, ATF-2, and other transcription factors (3,5).
Alternate Names
c-Jun N-terminal kinase 1; JNK; JNK-46; JNK1; JNK1 alpha protein kinase; JNK1 beta protein kinase; JNK1A2; JNK21B1/2; JUN N-terminal kinase; MAP kinase 8; MAPK 8; MAPK8; Mitogen-activated protein kinase 8; mitogen-activated protein kinase 8 isoform JNK1 alpha1; mitogen-activated protein kinase 8 isoform JNK1 beta2; MK08; PRKM8; protein kinase JNK1; SAPK1; SAPK1C; Stress-activated protein kinase 1; Stress-activated protein kinase 1c; Stress-activated protein kinase JNK1
