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FLASH GENE
Symbol FOS contributors: mct/npt/pgu - updated : 11-10-2015
HGNC name v-fos FBJ murine osteosarcoma viral oncogene homolog
HGNC id 3796
EXPRESSION
Type
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Nervousbraindiencephalonhypothalamussuprachiasmatic nuclei 
cell lineage
cell lines
fluid/secretion
at STAGE
physiological period fetal, pregnancy
Text term fetal membrane, amniotic cells, chorionic cells, fetal tooth germ cells
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • basic leucine zipper (bZIP) domain
  • a C terminal transactivation domain
  • mono polymer heteromer , dimer
    HOMOLOGY
    interspecies homolog to murine FBJ osteosarcoma viral (v-fos) oncogene
    Homologene
    FAMILY
  • bZIP family
  • Fos subfamily
  • CATEGORY transcription factor , protooncogene
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    intracellular,cytoplasm,cytosolic
    intracellular,nucleus,nucleoplasm
    intracellular,nucleus,chromatin/chromosome
    basic FUNCTION
  • putative gene regulator for cellular mechanism mediating neuronal excitability and survival
  • having tumour-suppressing and proapoptotic function in various cancer types
  • may undergo cell cycle dependent phosphorylation, in which some kinases including AURKA play a role in catalyzing the post translational modification of FOS
  • is able to regulate MZB cell development even in the absence of NOTCH2 5)
  • enhanced cytokine production and effector function of T cells may promote antitumor immunity when FOS fails to up-regulate PDCD1 during tumor progression
  • T-cell FOS subsequently induces PDCD1 expression in response to tumor progression
  • T-cell FOS expression promotes tumor growth following inoculation with tumor cells
  • suppresses antitumor T-cell function
  • FOS and RPS6 are induced by the biochemical activation of neurons, and therefore, these markers may be most responsive to stimuli that modulate neurons such as neuro-peptides and biogenic amines
  • critical cAMP effector, able to regulate the re-expression and splicing of epigenetically silenced genes associated with maturation (CD44) in retinoid-resistant NB4-LR1 leukemia cells
  • CELLULAR PROCESS cell life, proliferation/growth
    nucleotide, transcription
    PHYSIOLOGICAL PROCESS circadian , nervous system
    PATHWAY
    metabolism
    signaling signal transduction
    a component
  • forming heterodimers, the AP-1 complex with JUN family of proteins
  • INTERACTION
    DNA binding to the AP1 sequence of many genes
    RNA
    small molecule
    protein
  • interacting wwwith NR5A1, NR5A2 that are expressed in endometrial cancer
  • interacting with AURKA (Aurora-A is engaged in the regulation of FOS protein-protein interaction)
  • forms AP-1 transcription complexes with heterodimerization partners such as c-Jun, JunB, and JunD
  • bind to the promoters of a multitude of genes involved in critical cellular responses such as cell growth and proliferation, cell cycle regulation, embryonic development and cancer
  • interacting with KDM2B (KDM2B is an important anti-apoptotic molecule, which directly binds and represses FOS promoter in order for cancer cells to resist TRAIL-induced apoptosis)
  • NOTCH2 directly controls FOS transcription associated with Marginal zone B (MZB) cells development 5)
  • clear interaction between NOTCH2 and FOS, but the exact role of FOS in forming MZB cells has yet to be determined 5)
  • synthesis of FN1 is mediated by a transcriptional complex consisting of NFATC1, SP7 and FOS
  • dynamic interaction of SNAPC1 with elongating POLR2A during activation of the FOS gene by EGF
  • AFF2 is an upstream regulator of FOS and JUN, and further link deregulation of the immediate early response genes to the pathology of intellectual disability (ID)- and FRAXE-associated ID in particular
  • CARM1 represses replicative senescence by methylating ELAVL1 and thereby enhancing ELAVL1 ability to regulate the turnover of CCNA1, CCNB1, FOS, SIRT1, and CDKN2A mRNAs (
  • activation of the MAPK7/MAP2K5 pathway with CSF1R is required for osteoclast differentiation, which may induce differentiation through the induction of FOS
  • cell & other
    REGULATION
    activated by transiently by the binding sites to its SRE by SRF in cooperation with ATF6
    induced by light in the suprachiasmatic nucleus,SCN
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --low  
    associated with tumour progression in ovarian carcinoma and FOS may be a prognostic factor
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    cancer  
    early blockade of FOS–induced PDCD1 up-regulation may offer new opportunities for drug development for the prevention of many diseases, including cancer and chronic infection
    immunologyinfectious 
    early blockade of FOS–induced PDCD1 up-regulation may offer new opportunities for drug development for the prevention of many diseases, including chronic infection
    ANIMAL & CELL MODELS