In the field of molecular biology and Genetics, c-Fos is a protein encoded by the FOS gene.[1][2][3]
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c-Fos is a cellular proto-oncogene belonging to the immediate early gene family of transcription factors. c-Fos has a leucine-zipper DNA binding domain, and a transactivation domain at the C-terminus. Transcription of c-Fos is upregulated in response to many extracellular signals, e.g., growth factors. In addition, phosphorylation by MAPK, PKA, PKC or cdc2 alters the activity and stability of c-Fos. Members of the Fos family dimerise with C-jun to form the AP-1 transcription factor, which upregulates transcription of a diverse range of genes involved in everything from proliferation and differentiation to defense against invasion and cell damage.
The AP-1 complex has been implicated in transformation and progression of cancer, and both Fos and Jun were first discovered in rat fibroblasts. Fos was discovered as the transforming gene of the FBJ MSV and jun, first as the Fos-binding protein p39, then subsequently as the oncogene from avian sarcoma virus 17 (junana = 17).
The viral homologue of c-Fos, v-Fos, is found in the retrovirus Finkel–Biskis–Jinkins murine osteogenic sarcoma virus.
At least one study has shown that acute treatment with LSD is linked with a marked upregulation of c-fos expression in mammals.[4]
Neuroscientists measure expression of c-fos as an indirect marker of neuronal activity because c-fos is often expressed when neurons fire action potentials.[5][6] Upregulation of c-fos mRNA in a neuron indicates recent activity.[7]
C-Fos has been shown to interact with CSNK2A2,[8] Casein kinase 2, alpha 1,[8] BCL3,[9] DNA damage-inducible transcript 3,[10] Cofactor of BRCA1,[11] TATA binding protein,[12] RELA,[13] Nuclear receptor coactivator 1,[14][15] Nuclear receptor co-repressor 2,[16] RUNX2,[17][18] RUNX1,[17][18] C-jun[13][19][20][21][22][23][24] and Mothers against decapentaplegic homolog 3.[25]
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