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FBJ murine osteosarcoma viral oncogene homolog B also known as FOSB (in humans) or FosB (in other species) is a protein that, 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]

Delta FosBEdit

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] Delta FosB also regulates the commitment of mesenchymal precursor cells to the adipocyte or osteoblast lineage.[11]

Role in cocaine useEdit

Delta FosB levels have been found to increase upon the use of cocaine.[12] 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 led 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.

Transgenic mice exhibiting inducible expression of delta FosB primarily in the nucleus accumbens and dorsal striatum exhibit sensitized behavioural responses to drugs.[13] They self administer cocaine at lower doses than control,[14] but have a greater likelihood of relapse when the drug is withheld.[14][15] Delta FosB increases the expression of AMPA receptor subunit GluR2[13] and also decreases expression of dynorphin, thereby enhancing the sensitivity to reward.[15]

See alsoEdit


  1. 1.0 1.1 Entrez Gene: FOSB FBJ murine osteosarcoma viral oncogene homolog B.
  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.
  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.
  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.
  5. Werme M, Messer C, Olson L, et al. (2002). Delta FosB regulates wheel running. J. Neurosci. 22 (18): 8133–8.
  6. McClung CA, Nestler EJ (November 2003). Regulation of gene expression and cocaine reward by CREB and DeltaFosB. Nature Neuroscience 6 (11): 1208–15.
  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.
  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. Journal of Neuroscience 28 (29): 7344–9.
  9. Renthal W, Nestler EJ (August 2008). Epigenetic mechanisms in drug addiction. Trends in Molecular Medicine 14 (8): 341–50.
  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.
  11. Sabatakos G, Sims NA, Chen J, Aoki K, Kelz MB, Amling M, Bouali Y, Mukhopadhyay K, Ford K, Nestler EJ, Baron R (September 2000). Overexpression of DeltaFosB transcription factor(s) increases bone formation and inhibits adipogenesis.. Nature Medicine 6 (9): 985–90.
  12. Hope BT (May 1998). Cocaine and the AP-1 transcription factor complex. Ann. N. Y. Acad. Sci. 844: 1–6.
  13. 13.0 13.1 Kelz MB, Chen J, Carlezon WA, Whisler K, Gilden L, Beckmann AM, Steffen C, Zhang YJ, Marotti L, Self DW, Tkatch T, Baranauskas G, Surmeier DJ, Neve RL, Duman RS, Picciotto MR, Nestler EJ (September 1999). Expression of the transcription factor deltaFosB in the brain controls sensitivity to cocaine. Nature 401 (6750): 272–6.
  14. 14.0 14.1 Colby CR, Whisler K, Steffen C, Nestler EJ, Self DW (March 2003). Striatal cell type-specific overexpression of DeltaFosB enhances incentive for cocaine. J. Neurosci. 23 (6): 2488–93.
  15. 15.0 15.1 Nestler EJ, Barrot M, Self DW (September 2001). DeltaFosB: a sustained molecular switch for addiction. Proc. Natl. Acad. Sci. U.S.A. 98 (20): 11042–6.

Further readingEdit

  • 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.
  • 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.
  • Nakabeppu Y, Nathans D (1991). A naturally occurring truncated form of FosB that inhibits Fos/Jun transcriptional activity.. Cell 64 (4): 751–9.
  • Schuermann M, Jooss K, Müller R (1991). fosB is a transforming gene encoding a transcriptional activator.. Oncogene 6 (4): 567–76.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.

External linksEdit

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