NameMitogen-activated protein kinase 9
Synonyms
  • 2.7.11.24
  • c-Jun N-terminal kinase 2
  • JNK-55
  • JNK2
  • MAP kinase 9
  • PRKM9
  • SAPK1A
  • Stress-activated protein kinase 1a
  • Stress-activated protein kinase JNK2
Gene NameMAPK9
OrganismHuman
Amino acid sequence
>lcl|BSEQ0007238|Mitogen-activated protein kinase 9
MSDSKCDSQFYSVQVADSTFTVLKRYQQLKPIGSGAQGIVCAAFDTVLGINVAVKKLSRP
FQNQTHAKRAYRELVLLKCVNHKNIISLLNVFTPQKTLEEFQDVYLVMELMDANLCQVIH
MELDHERMSYLLYQMLCGIKHLHSAGIIHRDLKPSNIVVKSDCTLKILDFGLARTACTNF
MMTPYVVTRYYRAPEVILGMGYKENVDIWSVGCIMGELVKGCVIFQGTDHIDQWNKVIEQ
LGTPSAEFMKKLQPTVRNYVENRPKYPGIKFEELFPDWIFPSESERDKIKTSQARDLLSK
MLVIDPDKRISVDEALRHPYITVWYDPAEAEAPPPQIYDAQLEEREHAIEEWKELIYKEV
MDWEERSKNGVVKDQPSDAAVSSNATPSQSSSINDISSMSTEQTLASDTDSSLDASTGPL
EGCR
Number of residues424
Molecular Weight48138.655
Theoretical pI5.34
GO Classification
Functions
  • ATP binding
  • transcription factor binding
  • JUN kinase activity
  • cysteine-type endopeptidase activator activity involved in apoptotic process
Processes
  • positive regulation of apoptotic signaling pathway
  • Fc-epsilon receptor signaling pathway
  • toll-like receptor 9 signaling pathway
  • positive regulation of prostaglandin secretion
  • cellular response to tumor necrosis factor
  • toll-like receptor signaling pathway
  • toll-like receptor TLR1
  • regulation of circadian rhythm
  • positive regulation of transcription, DNA-templated
  • toll-like receptor TLR6
  • cellular response to growth factor stimulus
  • protein phosphorylation
  • TRIF-dependent toll-like receptor signaling pathway
  • central nervous system development
  • positive regulation of macrophage derived foam cell differentiation
  • response to toxic substance
  • cellular response to interleukin-1
  • protein targeting to mitochondrion
  • cellular response to lipopolysaccharide
  • positive regulation of nitric-oxide synthase biosynthetic process
  • positive regulation of nitric oxide biosynthetic process
  • neuron projection development
  • release of cytochrome c from mitochondria
  • MyD88-dependent toll-like receptor signaling pathway
  • positive regulation of prostaglandin biosynthetic process
  • regulation of JNK cascade
  • response to drug
  • MyD88-independent toll-like receptor signaling pathway
  • response to mechanical stimulus
  • cellular response to UV
  • regulation of sequence-specific DNA binding transcription factor activity
  • JNK cascade
  • regulation of protein ubiquitination
  • rhythmic process
  • stress-activated MAPK cascade
  • positive regulation of chemokine production
  • response to stress
  • toll-like receptor 10 signaling pathway
  • positive regulation of gene expression
  • positive regulation of cell morphogenesis involved in differentiation
  • toll-like receptor 2 signaling pathway
  • response to amine
  • toll-like receptor 3 signaling pathway
  • response to cadmium ion
  • innate immune response
  • toll-like receptor 4 signaling pathway
  • positive regulation of protein phosphorylation
  • toll-like receptor 5 signaling pathway
Components
  • mitochondrion
  • cytosol
  • nucleoplasm
General FunctionTranscription factor binding
Specific FunctionSerine/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).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.
Pfam Domain Function
Transmembrane RegionsNot Available
GenBank Protein ID598183
UniProtKB IDP45984
UniProtKB Entry NameMK09_HUMAN
Cellular LocationCytoplasm
Gene sequence
>lcl|BSEQ0021865|Mitogen-activated protein kinase 9 (MAPK9)
ATGAGCGACAGTAAATGTGACAGTCAGTTTTATAGTGTGCAAGTGGCAGACTCAACCTTC
ACTGTCCTAAAACGTTACCAGCAGCTGAAACCAATTGGCTCTGGGGCCCAAGGGATTGTT
TGTGCTGCATTTGATACAGTTCTTGGGATAAATGTTGCAGTCAAGAAACTAAGCCGTCCT
TTTCAGAACCAAACTCATGCAAAGAGAGCTTATCGTGAACTTGTCCTCTTAAAATGTGTC
AATCATAAAAATATAATTAGTTTGTTAAATGTGTTTACACCACAAAAAACTCTAGAAGAA
TTTCAAGATGTGTATTTGGTTATGGAATTAATGGATGCTAACTTATGTCAGGTTATTCAC
ATGGAGCTGGATCATGAAAGAATGTCCTACCTTCTTTACCAGATGCTTTGTGGTATTAAA
CATCTGCATTCAGCTGGTATAATTCATAGAGATTTGAAGCCTAGCAACATTGTTGTGAAA
TCAGACTGCACCCTGAAGATCCTTGACTTTGGCCTGGCCCGGACAGCGTGCACTAACTTC
ATGATGACCCCTTACGTGGTGACACGGTACTACCGGGCGCCCGAAGTCATCCTGGGTATG
GGCTACAAAGAGAACGTTGATATCTGGTCAGTGGGTTGCATCATGGGAGAGCTGGTGAAA
GGTTGTGTGATATTCCAAGGCACTGACCGTATCCTTCCCCGCGACCTTGGCCCCGCCATG
CTTTCTTAA
GenBank Gene IDL31951
GeneCard IDNot Available
GenAtlas IDNot Available
HGNC IDHGNC:6886
Chromosome Location5
Locus5q35
References
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