Mitogen-activated protein kinase 9, MAP kinase 9, MAPK 9, Stress-activated protein kinase 1a, SAPK1a, Stress-activated protein kinase JNK2, c-Jun N-terminal kinase 2, MAPK9, JNK2, PRKM9, SAPK1A
Recombinant human Mitogen-activated protein kinase 9 protein (1-424AA)
ELISA;Not yet tested in other applications.
Background / Function
Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK9/JNK2. In turn, MAPK9/JNK2 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity. In response to oxidative or ribotoxic stresses, inhibits rRNA synthesis by phosphorylating and inactivating the RNA polymerase 1-specific transcription initiation factor RRN3. Promotes stressed cell apoptosis by phosphorylating key regulatory factors including TP53 and YAP1. In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells. Upon T-cell receptor (TCR) stimulation, is activated by CARMA1, BCL10, MAP2K7 and MAP3K7/TAK1 to regulate JUN protein levels. Plays an important role in the osmotic stress-induced epithelial tight-junctions disruption. When activated, promotes beta-catenin/CTNNB1 degradation and inhibits the canonical Wnt signaling pathway. Participates also in neurite growth in spiral ganglion neurons. Phosphorylates the CLOCK-ARNTL/BMAL1 heterodimer and plays a role in the regulation of the circadian clock. MAPK9 isoforms display different binding patterns: alpha-1 and alpha-2 preferentially bind to 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 alpha-2, and JUND binds only weakly to it.
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, PH 7.4
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze.
Caprylic Acid Ammonium Sulfate Precipitation purified
Literature”Patterns of somatic mutation in human cancer genomes.”Greenman C., Stephens P., Smith R., Dalgliesh G.L., Hunter C., Bignell G., Davies H., Teague J., Butler A., Stevens C., Edkins S., O’Meara S., Vastrik I., Schmidt E.E., Avis T., Barthorpe S., Bhamra G., Buck G. Stratton M.R.Nature 446:153-158(2007). ”The crystal structure of JNK2 reveals conformational flexibility in the MAP kinase insert and indicates its involvement in the regulation of catalytic activity.”Shaw D., Wang S.M., Villasenor A.G., Tsing S., Walter D., Browner M.F., Barnett J., Kuglstatter A.J. Mol. Biol. 383:885-893(2008). ”JNK regulates the photic response of the mammalian circadian clock.” Yoshitane H., Honma S., Imamura K., Nakajima H., Nishide S.Y., Ono D., Kiyota H., Shinozaki N., Matsuki H., Wada N., Doi H., Hamada T., Honma K., Fukada Y. EMBO Rep. 13:455-461(2012).