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FBJ murine osteosarcoma viral oncogene homolog B
Identifiers
Symbols FOSB; DKFZp686C0818; G0S3; GOS3; GOSB; MGC42291
External IDs OMIM164772 MGI95575 HomoloGene31403 GeneCards: FOSB Gene
RNA expression pattern
PBB GE FOSB 202768 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 2354 14282
Ensembl ENSG00000125740 ENSMUSG00000003545
UniProt P53539 P13346
RefSeq (mRNA) NM_006732 NM_008036
RefSeq (protein) NP_006723 NP_032062
Location (UCSC) Chr 19:
50.66 - 50.67 Mb
Chr 7:
18.46 - 18.47 Mb
PubMed search [1] [2]

FBJ murine osteosarcoma viral oncogene homolog B also known as FOSB (in humans) or FosB (in other species) is a protein which in humans is encoded by the FOSB gene.[1][2][3]

The Fos gene family consists of 4 members: FOS, FOSB, FOSL1, and FOSL2. These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family, thereby forming the transcription factor complex AP-1. As such, the FOS proteins have been implicated as regulators of cell proliferation, differentiation, and transformation.[1]

Contents

Delta FosB

Delta FosB is a truncated splice variant of FosB.[4] Delta FosB has been implicated in the development of drug addiction and control of the reward system in the brain, and is linked to changes in a number of other gene products such as CREB and sirtuins.[5][6][7][8][9][10]

Role in cocaine use

"Delta FosB" levels have been found to increase upon the use of cocaine.[11] Each subsequent dose of cocaine will continue to increase the levels of Delta FosB with no ceiling of tolerance. Increasing the levels of Delta FosB has lead to increases in "Brain-Derived Neurotrophic Factor" (BDNF) levels, which in turn will increase the number of dendritic branches and spines present on neurons involved with the nucleus accumbens and prefrontal cortex areas of the brain. This change can be identified rather quickly, and may be sustained weeks after the last dose of the drug. This consequence of cocaine use may attribute to the idea of sensitization presented with the drug.

See also

References

  1. ^ a b "Entrez Gene: FOSB FBJ murine osteosarcoma viral oncogene homolog B". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=2354.  
  2. ^ Siderovski DP, Blum S, Forsdyke RE, Forsdyke DR (October 1990). "A set of human putative lymphocyte G0/G1 switch genes includes genes homologous to rodent cytokine and zinc finger protein-encoding genes". DNA Cell Biol. 9 (8): 579–87. doi:10.1089/dna.1990.9.579. PMID 1702972.  
  3. ^ Martin-Gallardo A, McCombie WR, Gocayne JD, FitzGerald MG, Wallace S, Lee BM, Lamerdin J, Trapp S, Kelley JM, Liu LI (April 1992). "Automated DNA sequencing and analysis of 106 kilobases from human chromosome 19q13.3". Nat. Genet. 1 (1): 34–9. doi:10.1038/ng0492-34. PMID 1301997.  
  4. ^ Nakabeppu Y, Nathans D (February 1991). "A naturally occurring truncated form of FosB that inhibits Fos/Jun transcriptional activity". Cell 64 (4): 751–9. doi:10.1016/0092-8674(91)90504-R. PMID 1900040.  
  5. ^ Werme M, Messer C, Olson L, et al. (2002). "Delta FosB regulates wheel running". J. Neurosci. 22 (18): 8133–8. PMID 12223567.  
  6. ^ McClung CA, Nestler EJ (November 2003). "Regulation of gene expression and cocaine reward by CREB and DeltaFosB". Nature Neuroscience 6 (11): 1208–15. doi:10.1038/nn1143. PMID 14566342.  
  7. ^ Nestler EJ (October 2008). "Review. Transcriptional mechanisms of addiction: role of DeltaFosB". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences 363 (1507): 3245–55. doi:10.1098/rstb.2008.0067. PMID 18640924.  
  8. ^ Renthal W, Carle TL, Maze I, Covington HE, Truong HT, Alibhai I, Kumar A, Montgomery RL, Olson EN, Nestler EJ (July 2008). "Delta FosB mediates epigenetic desensitization of the c-fos gene after chronic amphetamine exposure". The Journal of Neuroscience : the Official Journal of the Society for Neuroscience 28 (29): 7344–9. doi:10.1523/JNEUROSCI.1043-08.2008. PMID 18632938.  
  9. ^ Renthal W, Nestler EJ (August 2008). "Epigenetic mechanisms in drug addiction". Trends in Molecular Medicine 14 (8): 341–50. doi:10.1016/j.molmed.2008.06.004. PMID 18635399.  
  10. ^ Renthal W, Kumar A, Xiao G, Wilkinson M, Covington HE, Maze I, Sikder D, Robison AJ, LaPlant Q, Dietz DM, Russo SJ, Vialou V, Chakravarty S, Kodadek TJ, Stack A, Kabbaj M, Nestler EJ (May 2009). "Genome-wide analysis of chromatin regulation by cocaine reveals a role for sirtuins". Neuron 62 (3): 335–48. doi:10.1016/j.neuron.2009.03.026. PMID 19447090.  
  11. ^ Hope BT (May 1998). "Cocaine and the AP-1 transcription factor complex". Ann. N. Y. Acad. Sci. 844: 1–6. doi:10.1111/j.1749-6632.1998.tb08216.x. PMID 9668659.  

Further reading

  • Martin-Gallardo A, McCombie WR, Gocayne JD, et al. (1993). "Automated DNA sequencing and analysis of 106 kilobases from human chromosome 19q13.3.". Nat. Genet. 1 (1): 34–9. doi:10.1038/ng0492-34. PMID 1301997.  
  • Siderovski DP, Blum S, Forsdyke RE, Forsdyke DR (1991). "A set of human putative lymphocyte G0/G1 switch genes includes genes homologous to rodent cytokine and zinc finger protein-encoding genes.". DNA Cell Biol. 9 (8): 579–87. doi:10.1089/dna.1990.9.579. PMID 1702972.  
  • Nakabeppu Y, Nathans D (1991). "A naturally occurring truncated form of FosB that inhibits Fos/Jun transcriptional activity.". Cell 64 (4): 751–9. doi:10.1016/0092-8674(91)90504-R. PMID 1900040.  
  • Schuermann M, Jooss K, Müller R (1991). "fosB is a transforming gene encoding a transcriptional activator.". Oncogene 6 (4): 567–76. PMID 1903195.  
  • Brown JR, Ye H, Bronson RT, et al. (1996). "A defect in nurturing in mice lacking the immediate early gene fosB.". Cell 86 (2): 297–309. doi:10.1016/S0092-8674(00)80101-4. PMID 8706134.  
  • Heximer SP, Cristillo AD, Russell L, Forsdyke DR (1997). "Sequence analysis and expression in cultured lymphocytes of the human FOSB gene (G0S3).". DNA Cell Biol. 15 (12): 1025–38. doi:10.1089/dna.1996.15.1025. PMID 8985116.  
  • Liberati NT, Datto MB, Frederick JP, et al. (1999). "Smads bind directly to the Jun family of AP-1 transcription factors.". Proc. Natl. Acad. Sci. U.S.A. 96 (9): 4844–9. doi:10.1073/pnas.96.9.4844. PMID 10220381.  
  • Yamamura Y, Hua X, Bergelson S, Lodish HF (2000). "Critical role of Smads and AP-1 complex in transforming growth factor-beta -dependent apoptosis.". J. Biol. Chem. 275 (46): 36295–302. doi:10.1074/jbc.M006023200. PMID 10942775.  
  • Bergman MR, Cheng S, Honbo N, et al. (2003). "A functional activating protein 1 (AP-1) site regulates matrix metalloproteinase 2 (MMP-2) transcription by cardiac cells through interactions with JunB-Fra1 and JunB-FosB heterodimers.". Biochem. J. 369 (Pt 3): 485–96. doi:10.1042/BJ20020707. PMID 12371906.  
  • Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMID 12477932.  
  • Milde-Langosch K, Kappes H, Riethdorf S, et al. (2003). "FosB is highly expressed in normal mammary epithelia, but down-regulated in poorly differentiated breast carcinomas.". Breast Cancer Res. Treat. 77 (3): 265–75. doi:10.1023/A:1021887100216. PMID 12602926.  
  • Baumann S, Hess J, Eichhorst ST, et al. (2003). "An unexpected role for FosB in activation-induced cell death of T cells.". Oncogene 22 (9): 1333–9. doi:10.1038/sj.onc.1206126. PMID 12618758.  
  • Holmes DI, Zachary I (2004). "Placental growth factor induces FosB and c-Fos gene expression via Flt-1 receptors.". FEBS Lett. 557 (1-3): 93–8. doi:10.1016/S0014-5793(03)01452-2. PMID 14741347.  
  • Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMID 15489334.  
  • Konsman JP, Blomqvist A (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.  

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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