- CITATIONS: 1
|Application ||WB, IHC-P, E|
|Calculated MW||48139 Da|
|Antigen Region||349-379 aa|
|Other Names||Mitogen-activated protein kinase 9, MAP kinase 9, MAPK 9, JNK-55, Stress-activated protein kinase 1a, SAPK1a, Stress-activated protein kinase JNK2, c-Jun N-terminal kinase 2, MAPK9, JNK2, PRKM9, SAPK1A|
|Target/Specificity||This JNK2 (MAPK9) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 349-379 amino acids from the C-terminal region of human JNK2 (MAPK9).|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||JNK2 (MAPK9) Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||JNK2, PRKM9, SAPK1A|
|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 (PubMed:22441692).|
|Cellular Location||Cytoplasm. Nucleus|
Provided below are standard protocols that you may find useful for product applications.
JNK2 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: alpha-1 and alpha-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 alpha-2, and JUND binds only weakly to it. JNK2 is activated by threonine and tyrosine phosphorylation by either of two dual specificity kinases, MAP2K4 and MAP2K7. It is inhibited by dual specificity phosphatases, such as DUSP1. The protein has been shown to bind to at least three scaffolding proteins, MAPK8IP1/JIP-1, MAPK8IP2/JIP-2 and MAPK8IP3/JIP-3/JSAP1. These proteins also bind other components of the JNK signaling pathway
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Kallunki, T., et al., Genes Dev. 8(24):2996-3007 (1994).
Fleming, Y., et al., Biochem. J. 352 Pt 1, 145-154 (2000).
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