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Symbol MAPK8 contributors: shn - updated : 03-07-2017
HGNC name mitogen-activated protein kinase 8
HGNC id 6881
corresponding disease(s)
Other morbid association(s)
TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
constitutional       gain of function
in obesity
constitutional       loss of function
deficiency in the nervous system is sufficient to account for the role of MAPK8 in the regulation of high-fat diet-induced weight gain
Variant & Polymorphism
Candidate gene
Therapy target
  • JNK-related therapeutic strategies for RP1 diseases
  • SystemTypeDisorderPubmed
    a potential new therapy for diabetes using cell-permeable JNK-inhibitory peptide
    therapeutic target in abdominal aortic aneurysm
    JNK activity observed in wild-type activated TH cells was severely reduced in TH cells from Jnk1-/- mice
  • MAPK8 deficient mice display a progressive loss of axonal and dendritic microtubules and MAP1B and MAP2 are hypophosphorylated in MAPK8/ brains compromising their ability to bind to microtubules and promote their assembly and stability
  • Mice lacking both of the ubiquitously expressed isoforms JNK1 and -2 die during midgestation with neural tube closure defects and brain abnormalities
  • JNK-deficient mice exhibit delayed epithelial development in the epidermis, intestines, lungs, an eyelid closure defect associated with markedly reduced epidermal growth factor (EGF) receptor function, and loss of expression of the ligand EGF
  • genetic loss of the MAPK, c-Jun N-terminal kinase 1 in a mouse model of multiple sclerosis, enhances IL-10 production, rendering innate myeloid cells unresponsive to certain microbes and less capable of generating IL-17-roducing, encephalitogenic T cells