{"product_id":"abm218162","title":"Human Mitogen Activated Protein Kinase 9, MAPK9 ELISA Kit","description":"\u003ch3\u003eBackground\u003c\/h3\u003e\u003cp\u003eSerine\/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 (PubMed: 22441692). Phosphorylates POU5F1, which results in the inhibition of POU5F1's transcriptional activity and enhances its proteosomal degradation (By similarity). 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.\u003c\/p\u003e","brand":"BT LAB","offers":[{"title":"48T","offer_id":57661575922004,"sku":"ABM218162","price":205.0,"currency_code":"GBP","in_stock":true},{"title":"96T","offer_id":57661575954772,"sku":"ABM218163","price":293.0,"currency_code":"GBP","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/1040\/1782\/2036\/files\/btlab-7877a09ed6db22cf73c25d11acc4c53a4fa4aa3ee3ef6b9d5568978c00281bdb.jpg?v=1792159242","url":"https:\/\/www.abmium.com\/fr\/products\/abm218162","provider":"ABMIUM","version":"1.0","type":"link"}