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FLASH GENE

Symbol

FOS

contributors: mct/npt/pgu - updated : 11-10-2016

HGNC name	v-fos FBJ murine osteosarcoma viral oncogene homolog
HGNC id	3796

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_005252 4 - 2158 NP_005243 40.56 380 - 2009 19022561

EXPRESSION

Type

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Nervous brain diencephalon hypothalamus suprachiasmatic 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
	NQO1 directly interacts with the unstructured DNA-binding domain of FOS, which has been implicated in cancer proliferation, differentiation, and development as well as patient survival

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)

Type Gene Modification Chromosome rearrangement Protein expression Protein 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
	System Type Disorder Pubmed 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 immunology infectious   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