MAPK8

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Mitogen-activated protein kinase 8
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PDB rendering based on 1jnk.
Available structures: 1jnk, 1pmn, 1pmq, 1pmu, 1pmv, 1ukh, 1uki, 2b1p, 2exc, 2g01, 2gmx, 2h96, 2no3, 2o0u, 2o2u, 2ok1
Identifiers
Symbol(s) MAPK8; JNK; JNK1; JNK1A2; JNK21B1/2; PRKM8; SAPK1
External IDs OMIM: 601158 MGI1346861 Homologene56760
RNA expression pattern

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More reference expression data

Orthologs
Human Mouse
Entrez 5599 26419
Ensembl ENSG00000107643 ENSMUSG00000021936
Uniprot P45983 Q544A0
Refseq NM_002750 (mRNA)
NP_002741 (protein)
NM_016700 (mRNA)
NP_057909 (protein)
Location Chr 10: 49.18 - 49.32 Mb Chr 14: 32.21 - 32.28 Mb
Pubmed search [1] [2]

Mitogen-activated protein kinase 8, also known as MAPK8, is a human gene.


The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase is activated by various cell stimuli, and targets specific transcription factors, and thus mediates immediate-early gene expression in response to cell stimuli. The activation of this kinase by tumor-necrosis factor alpha (TNF-alpha) is found to be required for TNF-alpha induced apoptosis. This kinase is also involved in UV radiation induced apoptosis, which is thought to be related to cytochrom c-mediated cell death pathway. Studies of the mouse counterpart of this gene suggested that this kinase play a key role in T cell proliferation, apoptosis and differentiation. Four alternatively spliced transcript variants encoding distinct isoforms have been reported.[1]


References

Further reading

  • Davis RJ (2000). "Signal transduction by the JNK group of MAP kinases.". Cell 103 (2): 239-52. PMID 11057897.
  • Liu J, Lin A (2007). "Wiring the cell signaling circuitry by the NF-kappa B and JNK1 crosstalk and its applications in human diseases.". Oncogene 26 (22): 3267-78. doi:10.1038/sj.onc.1210417. PMID 17496921.

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


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