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Symbol JUN contributors: mct/pgu/shn - updated : 26-02-2016
HGNC name jun proto-oncogene
HGNC id 6204
corresponding disease(s)
Other morbid association(s)
TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
tumoral     --over  
in gastric cancer
constitutional     --over  
in in sudden infant death (in the brain)
tumoral     --over  
in breast cancer with liver metastasis
tumoral     --other  
dysregulation of JUN expression is a primary molecular aberrancy that contributes to the etiology and pathogenesis of juvenile myelomonocytic leukemia
Variant & Polymorphism
Candidate gene
Therapy target
opportunity for development of anti-JUN strategies in breast cancer therapy
potential pharmacologic interventions that may reduce JUN function or expression, (inhibition of JUN phosphorylation or expression could inhibit mutant PTPN11-induced monocytic differentiation) thus providing a novel therapeutic approach for juvenile myel
autoregulatory loop between JUN and FOSL1 might represent an important determinant for the increased JUN activity and a novel target for therapeutic intervention in tumorigenesis
  • mouse embryonic stem (ES) cells lacking c-Jun are viable and have a normal in vitro differentiation capacity
  • primary Jun-/- fibroblasts have a severe proliferation defect and undergo premature senescence in vitro
  • mouse primary JunAA (serines 63 and 73 mutated to alanines) fibroblasts have proliferation- and stress-induced apoptotic defects, accompanied by reduced AP-1 activity, and JunAA mice are viable and fertile, smaller than controls and resistant to epileptic seizures and neuronal apoptosis induced by the excitatory amino acid kainate
  • mouse primary hepatocytes lacking c-Jun showed increased sensitivity to TNF-alpha-induced apoptosis
  • embryos lacking c-Jun die at mid- to late-gestation and exhibit impaired hepatogenesis, altered fetal liver erythropoiesis and generalized oedema
  • Absence of mouse neuronal Jun reduced the speed of axonal regeneration following crush, and prevented most cut axons from reconnecting to their target, significantly reducing functional recovery (