c-fos gene、c-Fos protein

WordNet

the 3rd letter of the Roman alphabet (同)c
(music) the keynote of the scale of C major
a general-purpose programing language closely associated with the UNIX operating system
the 6th letter of the Roman alphabet (同)f

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carbonの化学記号
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/02/15 00:14:20」(JST)

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In the fields of molecular biology and genetics, c-Fos is a protein encoded by the FOS gene.^[1]^[2]^[3]

Structure and function

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.

Clinical significance

The AP-1 complex has been implicated in transformation and progression of cancer, and both c-Fos and c-Jun were first discovered in rat fibroblasts. C-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.

Cocaine, methamphetamine,^[4] heroin,^[5] and other psychoactive drugs^[6]^[7] have been shown to increase c-fos production in prefrontal cortex as well as in the mesolimbic reward pathway. As such, the c-Fos promoter finds utilization in drug abuse research in general, as well as with context-induced relapse to drug-seeking and other behavioral changes associated with chronic drug taking.

An increase in c-Fos production in androgen receptor-containing neurons has been observed in rats after mating.

Applications

Expression of c-fos is an indirect marker of neuronal activity because c-fos is often expressed when neurons fire action potentials.^[8]^[9] Upregulation of c-fos mRNA in a neuron indicates recent activity.^[10]

Drug abuse research also finds application of the c-fos promoter. Scientists use this promoter to turn on transgenes in rats that allow them to manipulate specific neuronal ensembles to assess their role in drug-related memories and behavior.^[11] This neuronal control can be replicated with optogenetics or DREADDs.

Interactions

C-Fos has been shown to interact with:

BCL3,^[12]
COBRA1,^[13]
CSNK2A1,^[14]
CSNK2A2,^[14]
DDIT3,^[15]
JUN^[16]^[17]^[18]^[19]^[20]^[21]^[22]
NCOA1;,^[23]^[24]
NCOR2,^[25]
RELA,^[16]
RUNX1,^[26]^[27]
RUNX2,^[26]^[27]
SMAD3,^[28] and
TBP.^[29]

References

^ Monje P, Hernández-Losa J, Lyons RJ, Castellone MD, Gutkind JS (October 2005). "Regulation of the transcriptional activity of c-Fos by ERK. A novel role for the prolyl isomerase PIN1". J. Biol. Chem. 280 (42): 35081–4. doi:10.1074/jbc.C500353200. PMID 16123044.
^ Bossis G, Malnou CE, Farras R, Andermarcher E, Hipskind R, Rodriguez M, Schmidt D, Muller S, Jariel-Encontre I, Piechaczyk M (August 2005). "Down-Regulation of c-Fos/c-Jun AP-1 Dimer Activity by Sumoylation". Mol. Cell. Biol. 25 (16): 6964–79. doi:10.1128/MCB.25.16.6964-6979.2005. PMC 1190241. PMID 16055710. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1190241/.
^ Konsman JP, Blomqvist A (May 2005). "Forebrain patterns of c-Fos and FosB induction during cancer-associated anorexia-cachexia in rat". Eur. J. Neurosci. 21 (10): 2752–66. doi:10.1111/j.1460-9568.2005.04102.x. PMID 15926923.
^ Graybiel AM, Moratalla R, Robertson HA (September 1990). "Amphetamine and cocaine induce drug-specific activation of the c-fos gene in striosome-matrix compartments and limbic subdivisions of the striatum". Proc. Natl. Acad. Sci. U.S.A. 87 (17): 6912–6. doi:10.1073/pnas.87.17.6912. PMC 54648. PMID 2118661. //www.ncbi.nlm.nih.gov/pmc/articles/PMC54648/.
^ Curran EJ, Akil H, Watson SJ (November 1996). "Psychomotor stimulant- and opiate-induced c-fos mRNA expression patterns in the rat forebrain: comparisons between acute drug treatment and a drug challenge in sensitized animals". Neurochem. Res. 21 (11): 1425–35. doi:10.1007/BF02532384. PMID 8947933.
^ Nichols CD, Sanders-Bush E (May 2002). "A single dose of lysergic acid diethylamide influences gene expression patterns within the mammalian brain". Neuropsychopharmacology 26 (5): 634–42. doi:10.1016/S0893-133X(01)00405-5. PMID 11927188.
^ Singewald N, Salchner P, Sharp T (February 2003). "Induction of c-Fos expression in specific areas of the fear circuitry in rat forebrain by anxiogenic drugs". Biol. Psychiatry 53 (4): 275–83. doi:10.1016/S0006-3223(02)01574-3. PMID 12586446.
^ VanElzakker M, Fevurly RD, Breindel T, Spencer RL (2008). "Environmental novelty is associated with a selective increase in Fos expression in the output elements of the hippocampal formation and the perirhinal cortex". Learn. Mem. 15 (12): 899–908. doi:10.1101/lm.1196508. PMC 2632843. PMID 19050162. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2632843/.
^ Dragunow M, Faull R (1989). "The use of c-fos as a metabolic marker in neuronal pathway tracing". Journal of Neuroscience Methods 29 (3): 261–265. doi:10.1016/0165-0270(89)90150-7. PMID 2507830.
^ Day HE, Kryskow EM, Nyhuis TJ, Herlihy L, Campeau S (September 2008). "Conditioned Fear Inhibits c-fos mRNA Expression in the Central Extended Amygdala". Brain Res. 1229: 137–46. doi:10.1016/j.brainres.2008.06.085. PMC 2605076. PMID 18634767. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2605076/.
^ Koya E, Golden SA, Harvey BK, Guez-Barber DH, Berkow A, Simmons DE, Bossert JM, Nair SG, Uejima JL, Marin MT, Mitchell TB, Farquhar D, Ghosh SC, Mattson BJ, Hope BT (August 2009). "Targeted disruption of cocaine-activated nucleus accumbens neurons prevents context-specific sensitization". Nat. Neurosci. 12 (8): 1069–73. doi:10.1038/nn.2364. PMC 2752202. PMID 19620976. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2752202/.
^ Na SY, Choi JE, Kim HJ, Jhun BH, Lee YC, Lee JW (October 1999). "Bcl3, an IkappaB protein, stimulates activating protein-1 transactivation and cellular proliferation". J. Biol. Chem. 274 (40): 28491–6. doi:10.1074/jbc.274.40.28491. PMID 10497212.
^ Zhong H, Zhu J, Zhang H, Ding L, Sun Y, Huang C, Ye Q (December 2004). "COBRA1 inhibits AP-1 transcriptional activity in transfected cells". Biochem. Biophys. Res. Commun. 325 (2): 568–73. doi:10.1016/j.bbrc.2004.10.079. PMID 15530430.
^ ^a ^b Yamaguchi Y, Wada T, Suzuki F, Takagi T, Hasegawa J, Handa H (August 1998). "Casein kinase II interacts with the bZIP domains of several transcription factors". Nucleic Acids Res. 26 (16): 3854–61. doi:10.1093/nar/26.16.3854. PMC 147779. PMID 9685505. //www.ncbi.nlm.nih.gov/pmc/articles/PMC147779/.
^ Ubeda M, Vallejo M, Habener JF (November 1999). "CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins". Mol. Cell. Biol. 19 (11): 7589–99. PMC 84780. PMID 10523647. //www.ncbi.nlm.nih.gov/pmc/articles/PMC84780/.
^ ^a ^b Yang X, Chen Y, Gabuzda D (September 1999). "ERK MAP kinase links cytokine signals to activation of latent HIV-1 infection by stimulating a cooperative interaction of AP-1 and NF-kappaB". J. Biol. Chem. 274 (39): 27981–8. doi:10.1074/jbc.274.39.27981. PMID 10488148.
^ Ito T, Yamauchi M, Nishina M, Yamamichi N, Mizutani T, Ui M, Murakami M, Iba H (January 2001). "Identification of SWI.SNF complex subunit BAF60a as a determinant of the transactivation potential of Fos/Jun dimers". J. Biol. Chem. 276 (4): 2852–7. doi:10.1074/jbc.M009633200. PMID 11053448.
^ Pognonec P, Boulukos KE, Aperlo C, Fujimoto M, Ariga H, Nomoto A, Kato H (May 1997). "Cross-family interaction between the bHLHZip USF and bZip Fra1 proteins results in down-regulation of AP1 activity". Oncogene 14 (17): 2091–8. doi:10.1038/sj.onc.1201046. PMID 9160889.
^ Glover JN, Harrison SC (January 1995). "Crystal structure of the heterodimeric bZIP transcription factor c-Fos-c-Jun bound to DNA". Nature 373 (6511): 257–61. doi:10.1038/373257a0. PMID 7816143.
^ Nomura N, Zu YL, Maekawa T, Tabata S, Akiyama T, Ishii S (February 1993). "Isolation and characterization of a novel member of the gene family encoding the cAMP response element-binding protein CRE-BP1". J. Biol. Chem. 268 (6): 4259–66. PMID 8440710.
^ Finkel T, Duc J, Fearon ER, Dang CV, Tomaselli GF (January 1993). "Detection and modulation in vivo of helix-loop-helix protein-protein interactions". J. Biol. Chem. 268 (1): 5–8. PMID 8380166.
^ Venugopal R, Jaiswal AK (December 1998). "Nrf2 and Nrf1 in association with Jun proteins regulate antioxidant response element-mediated expression and coordinated induction of genes encoding detoxifying enzymes". Oncogene 17 (24): 3145–56. doi:10.1038/sj.onc.1202237. PMID 9872330.
^ Lee SK, Na SY, Jung SY, Choi JE, Jhun BH, Cheong J, Meltzer PS, Lee YC, Lee JW (June 2000). "Activating protein-1, nuclear factor-kappaB, and serum response factor as novel target molecules of the cancer-amplified transcription coactivator ASC-2". Mol. Endocrinol. 14 (6): 915–25. doi:10.1210/me.14.6.915. PMID 10847592.
^ Lee SK, Kim HJ, Na SY, Kim TS, Choi HS, Im SY, Lee JW (July 1998). "Steroid receptor coactivator-1 coactivates activating protein-1-mediated transactivations through interaction with the c-Jun and c-Fos subunits". J. Biol. Chem. 273 (27): 16651–4. doi:10.1074/jbc.273.27.16651. PMID 9642216.
^ Lee SK, Kim JH, Lee YC, Cheong J, Lee JW (April 2000). "Silencing mediator of retinoic acid and thyroid hormone receptors, as a novel transcriptional corepressor molecule of activating protein-1, nuclear factor-kappaB, and serum response factor". J. Biol. Chem. 275 (17): 12470–4. doi:10.1074/jbc.275.17.12470. PMID 10777532.
^ ^a ^b Hess J, Porte D, Munz C, Angel P (June 2001). "AP-1 and Cbfa/runt physically interact and regulate parathyroid hormone-dependent MMP13 expression in osteoblasts through a new osteoblast-specific element 2/AP-1 composite element". J. Biol. Chem. 276 (23): 20029–38. doi:10.1074/jbc.M010601200. PMID 11274169.
^ ^a ^b D'Alonzo RC, Selvamurugan N, Karsenty G, Partridge NC (January 2002). "Physical interaction of the activator protein-1 factors c-Fos and c-Jun with Cbfa1 for collagenase-3 promoter activation". J. Biol. Chem. 277 (1): 816–22. doi:10.1074/jbc.M107082200. PMID 11641401.
^ Zhang Y, Feng XH, Derynck R (August 1998). "Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-beta-induced transcription". Nature 394 (6696): 909–13. doi:10.1038/29814. PMID 9732876.
^ Metz R, Bannister AJ, Sutherland JA, Hagemeier C, O'Rourke EC, Cook A, Bravo R, Kouzarides T (September 1994). "c-Fos-induced activation of a TATA-box-containing promoter involves direct contact with TATA-box-binding protein". Mol. Cell. Biol. 14 (9): 6021–9. doi:10.1128/MCB.14.9.6021. PMC 359128. PMID 8065335. //www.ncbi.nlm.nih.gov/pmc/articles/PMC359128/.

External links

c-fos+Proteins at the US National Library of Medicine Medical Subject Headings (MeSH)
c-fos+Genes at the US National Library of Medicine Medical Subject Headings (MeSH)
FactorBook C-Fos
Drosophila kayak - The Interactive Fly

UpToDate Contents

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English Journal

Valproate ameliorates nitroglycerin-induced migraine in trigeminal nucleus caudalis in rats through inhibition of NF-кB.

Li Y1, Zhang Q1, Qi D1, Zhang L1, Yi L1, Li Q1, Zhang Z2.
The journal of headache and pain.J Headache Pain.2016 Dec;17(1):49. doi: 10.1186/s10194-016-0631-z. Epub 2016 May 6.
BACKGROUND: As a complex nervous system disease, migraine causes severe healthy and social issues worldwide. Valproate (VPA) is a widely used treatment agent against seizures and bipolar disorder, and its function to alleviate damage due to migraine has also been verified in clinical investigations.
PMID 27150105

Social predisposition dependent neuronal activity in the intermediate medial mesopallium of domestic chicks (Gallus gallus domesticus).

Mayer U1, Rosa-Salva O2, Lorenzi E2, Vallortigara G2.
Behavioural brain research.Behav Brain Res.2016 Sep 1;310:93-102. doi: 10.1016/j.bbr.2016.05.019. Epub 2016 May 9.
Species from phylogenetically distant animal groups, such as birds and primates including humans, share early experience-independent social predispositions that cause offspring, soon after birth, to attend to and learn about conspecifics. One example of this phenomenon is provided by the behaviour o
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Neuronal activity and the expression of hypothalamic oxytocin and vasopressin in social versus cocaine conditioning.

Liu C1, Wang J2, Zhan B1, Cheng G1.
Behavioural brain research.Behav Brain Res.2016 Sep 1;310:84-92. doi: 10.1016/j.bbr.2016.05.010. Epub 2016 May 9.
Although drug rewards and natural rewards share neural substrates, the neuronal activation patterns and mechanisms behind the interaction between cocaine and social reward are poorly understood. Here, we investigated the conditioned place preference (CPP) in social (conspecific) vs cocaine condition
PMID 27163750

Japanese Journal

Purslane Suppresses Osteoclast Differentiation and Bone Resorbing Activity via Inhibition of Akt/GSK3β-c-Fos-NFATc1 Signaling in Vitro and Prevents Lipopolysaccharide-Induced Bone Loss in Vivo

Kim Ju-Young,Oh Hyun Mee,Kwak Sung Chul [他]
Biological & pharmaceutical bulletin 38(1), 66-74, 2015-01
NAID 40020311858

Assessment of intraoral mucosal pain induced by the application of capsaicin

Terayama Ryuji,Maruhama Kotaro,Tsuchiya Hiroki,Mizutani Masahide,Iida Seiji,Sugimoto Tomosada
Archives of Oral Biology 59(12), 1334-1341, 2014-12
… The number of c-Fos protein-like immunoreactive (Fos-LI) neurons in the medullary dorsal horn (MDH) induced by the intraoral application of capsaicin was measured. …
NAID 120005477122

The regulation of hepcidin expression by serum treatment: requirements of the BMP response element and STAT- and AP-1-binding sites.

Kanamori Yohei,Murakami Masaru,Matsui Tohru,Funaba Masayuki
Gene 551(2), 119-126, 2014-11-10
… Serum treatment induced the expression of the AP-1 components c-fos and junB in primary hepatocytes and HepG2 cells. … Forced expression of c-fos or junB enhanced the response of hepcidin transcription to serum treatment. … By contrast, the expression of dominant negative (dn)-c-fos and dn-junB decreased hepcidin transcription. …
NAID 120005511083

Related Pictures

Rabbit c-Fos and mouse GFAP antibodies from EnCor Rabbit c-Fos and Chicken vimentin Antibodies from EnCor #2 c-Fos 抗体 | 抗体すべての製造業者からの製品情報 c-Fos Antibody (NB110-75039): Novus Biologicals Anti-c-Fos antibody (ab190289) | Abcam c-Fos Antibody (H-125) | Santa Cruz Biotech c-Fos Antibody (D-1) | Santa Cruz Biotech c-FOS Antibody 26192-1-AP | Proteintech

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拡張検索	「c-Fos protein」「proto-oncogene protein c-Fos」「癌原遺伝子産物c-Fos」「c-Fosタンパク質」
関連記事	「C」「F」「c」

「c-Fos protein」

FBJ murine osteosarcoma viral oncogene homolog
	; PDB rendering based on 1a02.
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1A02, 1FOS, 1S9K
Identifiers
Symbols	FOS; AP-1; C-FOS; p55
External IDs	OMIM: 164810 MGI: 95574 HomoloGene: 3844 ChEMBL: 5029 GeneCards: FOS Gene
Gene Ontology
Molecular function	• double-stranded DNA binding; • sequence-specific DNA binding transcription factor activity; • protein binding; • sequence-specific DNA binding; • transcription regulatory region DNA binding; • R-SMAD binding;
Cellular component	• nucleus; • nucleoplasm; • transcription factor complex; • nucleolus;
Biological process	• conditioned taste aversion; • toll-like receptor signaling pathway; • MyD88-dependent toll-like receptor signaling pathway; • MyD88-independent toll-like receptor signaling pathway; • DNA methylation; • regulation of transcription from RNA polymerase II promoter; • transcription from RNA polymerase II promoter; • inflammatory response; • transforming growth factor beta receptor signaling pathway; • nervous system development; • female pregnancy; • aging; • Toll signaling pathway; • response to cold; • response to light stimulus; • response to mechanical stimulus; • response to gravity; • response to toxin; • sleep; • cellular response to extracellular stimulus; • response to lipopolysaccharide; • response to progesterone stimulus; • cellular response to hormone stimulus; • response to cytokine stimulus; • toll-like receptor 1 signaling pathway; • toll-like receptor 2 signaling pathway; • toll-like receptor 3 signaling pathway; • toll-like receptor 4 signaling pathway; • cellular response to reactive oxygen species; • TRIF-dependent toll-like receptor signaling pathway; • response to drug; • innate immune response; • positive regulation of transcription, DNA-dependent; • positive regulation of transcription from RNA polymerase II promoter; • regulation of sequence-specific DNA binding transcription factor activity; • stress-activated MAPK cascade; • response to corticosterone stimulus; • response to cAMP; • SMAD protein signal transduction; • cellular response to calcium ion;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
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