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Gene Review

FOSL2  -  FOS-like antigen 2

Homo sapiens

Synonyms: FLJ23306, FRA-2, FRA2, Fos-related antigen 2
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Disease relevance of FOSL2


High impact information on FOSL2

  • The nontransforming proteins Fra1 and Fra2 can be converted to transforming proteins by fusion of a transactivation domain from either FosB or VP16 [5].
  • In contrast, PTX-B inhibited AP-1 binding to target DNA and modified its composition with a proportional increases in FosB, Fra2, and ATF2 [6].
  • Utrophin enhancer activity was dependent on an AP-1 site, and in satellite cells of regenerating muscle the AP-1 factors Fra1, Fra2, and JunD were strongly induced [7].
  • In untreated cells, SPRR1B promoter is predominantly occupied by JunD and Fra2 [8].
  • Avian primary cells transformed by either Jun : Fra2 or Jun : ATF2 thus provide powerful tools for the investigation of the downstream pathways involved in oncogenesis [9].

Biological context of FOSL2


Anatomical context of FOSL2

  • Intriguingly, overexpression of fra2 suppressed PMA-inducible reporter activity, whereas fra1 significantly enhanced basal level activity, indicating an opposing role for these proteins in SPRR1B expression in a manner similar to that observed in proximal tracheobronchial epithelial cells (BEAS-2B clone S6) [11].
  • Four proteins (FBR-v-Fos, FBJ-v-Fos, c-Fos, and FosB) transform established rodent fibroblast cell lines, while three (FosB2, Fra1, and Fra2) do not [5].
  • Interestingly, most AP-1 factors were expressed in the intermediate (extravillous) trophoblast, with expression being strongest for JunD and Fra2 (100% of nuclei showing strong expression), followed by c-Jun (80% positive nuclei), c-Fos and FosB (50% positive nuclei) [12].
  • High levels of fra-2 mRNA were detected in ovary, stomach, small and large intestine, brain, lung and heart [13].
  • RESULTS: Transcriptionally active AP-1 in combinations of c-Jun, JunD and JunB with Fra1, Fra2 and possibly FosB, are expressed in cardiac myocytes [14].

Associations of FOSL2 with chemical compounds

  • FRA-2 protein represented the main component of the chronic amphetamine- or cocaine-activated complexes, which suggests its relevance in the long-term effects of psychostimulant drugs [15].
  • Proteasomal inhibition, which reduced the NE-stimulated induction of aa-nat, caused a reduction of ICER and Fra-2 [16].
  • Our laboratory has discovered that Fos-related antigen-2 from AP-1 transcription factor family and NF-kappa B p65 and p50 subunits are induced long-term (days to months) in the brain after neurotoxic, excitotoxic or ischemic insult [17].

Other interactions of FOSL2

  • PMA significantly induced binding of JunB and Fra1 in normal cells, while JunB and Fra2 bound to TREs in the malignant cells [8].
  • RESULTS: Of the seven AP-1 factors, three (c-fos, fra2, and junB) clearly showed higher expression levels in tumors when compared to matched normal endometrial samples [18].
  • This TRE bound TPA induced specific nuclear complexes in vitro containing junD, c-jun, c-fos, and fra2 but not cAMP-responsive element binding/activating transcription factor family proteins [19].

Analytical, diagnostic and therapeutic context of FOSL2

  • Of the 352 differentially expressed genes found, CD70 and FRA2 were selected for further evaluation by real-time RT-PCR [20].


  1. Chromosomal assignment of the human gene encoding the Fos-related antigen-2 (FRA2) to chromosome 2p22-p23. Molven, A., Houge, G., Berger, R. Genomics (1996) [Pubmed]
  2. HMG-I(Y) and the CBP/p300 coactivator are essential for human papillomavirus type 18 enhanceosome transcriptional activity. Bouallaga, I., Teissier, S., Yaniv, M., Thierry, F. Mol. Cell. Biol. (2003) [Pubmed]
  3. Expression pattern of the AP-1 family in breast cancer: association of fosB expression with a well-differentiated, receptor-positive tumor phenotype. Bamberger, A.M., Methner, C., Lisboa, B.W., Städtler, C., Schulte, H.M., Löning, T., Milde-Langosch, K. Int. J. Cancer (1999) [Pubmed]
  4. Expression pattern of the activating protein-1 family of transcription factors in gestational trophoblastic lesions. Briese, J., Sudahl, S., Schulte, H.M., Löning, T., Bamberger, A.M. Int. J. Gynecol. Pathol. (2005) [Pubmed]
  5. Transformation by Fos proteins requires a C-terminal transactivation domain. Wisdon, R., Verma, I.M. Mol. Cell. Biol. (1993) [Pubmed]
  6. Pertussis toxin B-oligomer suppresses IL-6 induced HIV-1 and chemokine expression in chronically infected U1 cells via inhibition of activator protein 1. Rizzi, C., Crippa, M.P., Jeeninga, R.E., Berkhout, B., Blasi, F., Poli, G., Alfano, M. J. Immunol. (2006) [Pubmed]
  7. The utrophin gene is transcriptionally up-regulated in regenerating muscle. Galvagni, F., Cantini, M., Oliviero, S. J. Biol. Chem. (2002) [Pubmed]
  8. Mechanism of repression of squamous differentiation marker, SPRR1B, in malignant bronchial epithelial cells: role of critical TRE-sites and its transacting factors. Patterson, T., Vuong, H., Liaw, Y.S., Wu, R., Kalvakolanu, D.V., Reddy, S.P. Oncogene (2001) [Pubmed]
  9. Distinct roles of Jun : Fos and Jun : ATF dimers in oncogenesis. van Dam, H., Castellazzi, M. Oncogene (2001) [Pubmed]
  10. Opposing functions of ATF2 and Fos-like transcription factors in c-Jun-mediated myogenin expression and terminal differentiation of avian myoblasts. Daury, L., Busson, M., Tourkine, N., Casas, F., Cassar-Malek, I., Wrutniak-Cabello, C., Castellazzi, M., Cabello, G. Oncogene (2001) [Pubmed]
  11. JNK1 and AP-1 regulate PMA-inducible squamous differentiation marker expression in Clara-like H441 cells. Vuong, H., Patterson, T., Adiseshaiah, P., Shapiro, P., Kalvakolanu, D.V., Reddy, S.P. Am. J. Physiol. Lung Cell Mol. Physiol. (2002) [Pubmed]
  12. Expression pattern of the activating protein-1 family of transcription factors in the human placenta. Bamberger, A.M., Bamberger, C.M., Aupers, S., Milde-Langosch, K., Löning, T., Makrigiannakis, A. Mol. Hum. Reprod. (2004) [Pubmed]
  13. Cloning and characterisation of the mouse fra-2 gene. Foletta, V.C., Sonobe, M.H., Suzuki, T., Endo, T., Iba, H., Cohen, D.R. Oncogene (1994) [Pubmed]
  14. Hypertrophic agonists induce the binding of c-Fos to an AP-1 site in cardiac myocytes: implications for the expression of GLUT1. Santalucía, T., Christmann, M., Yacoub, M.H., Brand, N.J. Cardiovasc. Res. (2003) [Pubmed]
  15. Effect of acute and chronic psychostimulant drugs on redox status, AP-1 activation and pro-enkephalin mRNA in the human astrocyte-like U373 MG cells. Malaplate-Armand, C., Becuwe, P., Ferrari, L., Masson, C., Dauça, M., Visvikis, S., Lambert, H., Batt, A.M. Neuropharmacology (2005) [Pubmed]
  16. The role of inducible repressor proteins in the adrenergic induction of arylalkylamine-N-acetyltransferase and mitogen-activated protein kinase phosphatase-1 in rat pinealocytes. Ho, A.K., Terriff, D.L., Price, D.M., Wloka, M.T., Chik, C.L. Endocrinology (2007) [Pubmed]
  17. Brain injury: prolonged induction of transcription factors. Pennypacker, K.R., Kassed, C.A., Eidizadeh, S., O'Callaghan, J.P. Acta neurobiologiae experimentalis. (2000) [Pubmed]
  18. Expression pattern of the AP-1 family in endometrial cancer: correlations with cell cycle regulators. Bamberger, A.M., Milde-Langosch, K., Rössing, E., Goemann, C., Löning, T. J. Cancer Res. Clin. Oncol. (2001) [Pubmed]
  19. Transcriptional regulation of intercellular adhesion molecule 1 by phorbol ester in human neuroblastoma cell line SK-N-SH involves jun- and fos-containing activator protein 1 site binding complex(es). Farina, A.R., Cappabianca, L., Mackay, A.R., Tiberio, A., Tacconelli, A., Tessitore, A., Frati, L., Martinotti, S., Gulino, A. Cell Growth Differ. (1997) [Pubmed]
  20. Identification of CD70 as a diagnostic biomarker for clear cell renal cell carcinoma by gene expression profiling, real-time RT-PCR and immunohistochemistry. Diegmann, J., Junker, K., Gerstmayer, B., Bosio, A., Hindermann, W., Rosenhahn, J., von Eggeling, F. Eur. J. Cancer (2005) [Pubmed]
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