Polyclonal Antibody to JNK1/JNK2/JNK3 (phospho-Thr183/Tyr185)

Responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity. In T-cells, JNK1 and JNK2 are required for polarized differentiation of T-helper cells into Th1 cells By similarity. Phosphorylates heat shock factor protein 4 (HSF4) . /Responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, primarily components of AP-1 such as c-Jun and ATF2 and thus regulates AP-1 transcriptional activity. In T-cells, JNK1 and JNK2 are required for polarized differentiation of T-helper cells into Th1 cells. JNK2 isoforms display different binding patterns: a-1 and a-2 preferentially bind to c-Jun, whereas beta-1 and beta-2 bind to ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms. JUNB is not a substrate for JNK2 a-2, and JUND binds only weakly to it. /Responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, primarily components of AP-1 such as c-Jun and ATF2 and thus regulates AP-1 transcriptional activity. Required for stress-induced neuronal apoptosis and the pathogenesis of glutamate excitotoxicity Davis, R.J. (1999) Biochem Soc Symp 64, 1-12. Ichijo, H. (1999) Oncogene 18, 6087-93. Kyriakis, J.M. and Avruch, J. (2001) Physiol Rev 81, 807-69.