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NM_005253

NM_008037
RefSeq (protein)

NP_005244

NP_032063
Location (UCSC) Chr 2: 28.39 – 28.42 Mb Chr 5: 32.14 – 32.16 Mb PubMed search [3] [4] Wikidata
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Fos-related antigen 2 (FRA2) is a protein that in humans is encoded by the FOSL2 gene.[5]

Function

The Fos gene family consists of 4 members: c-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.[5]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000075426 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000029135 - Ensembl, May 2017
  3. ^ "Human PubMed Reference:". 
  4. ^ "Mouse PubMed Reference:". 
  5. ^ a b "Entrez Gene: FOSL2 FOS-like antigen 2". 

Further reading

  • Matsui M, Tokuhara M, Konuma Y, Nomura N, Ishizaki R (March 1990). "Isolation of human fos-related genes and their expression during monocyte-macrophage differentiation". Oncogene. 5 (3): 249–55. PMID 2107490. 
  • Molven A, Houge G, Berger R (November 1996). "Chromosomal assignment of the human gene encoding the Fos-related antigen-2 (FRA2) to chromosome 2p22-p23". Genomics. 38 (1): 72–5. doi:10.1006/geno.1996.0593. PMID 8954781. 
  • Outinen PA, Sood SK, Pfeifer SI, Pamidi S, Podor TJ, Li J, Weitz JI, Austin RC (August 1999). "Homocysteine-induced endoplasmic reticulum stress and growth arrest leads to specific changes in gene expression in human vascular endothelial cells". Blood. 94 (3): 959–67. PMID 10419887. 
  • Miyamoto NG, Medberry PS, Hesselgesser J, Boehlk S, Nelson PJ, Krensky AM, Perez HD (June 2000). "Interleukin-1beta induction of the chemokine RANTES promoter in the human astrocytoma line CH235 requires both constitutive and inducible transcription factors". Journal of Neuroimmunology. 105 (1): 78–90. doi:10.1016/S0165-5728(00)00195-8. PMID 10713367. 
  • Ng DC, Shafaee S, Lee D, Bikle DD (August 2000). "Requirement of an AP-1 site in the calcium response region of the involucrin promoter". The Journal of Biological Chemistry. 275 (31): 24080–8. doi:10.1074/jbc.M002508200. PMID 10816578. 
  • Bamberger AM, Milde-Langosch K, Rössing E, Goemann C, Löning T (September 2001). "Expression pattern of the AP-1 family in endometrial cancer: correlations with cell cycle regulators". Journal of Cancer Research and Clinical Oncology. 127 (9): 545–50. doi:10.1007/s004320100255. PMID 11570575. 
  • Udalova IA, Kwiatkowski D (November 2001). "Interaction of AP-1 with a cluster of NF-kappa B binding elements in the human TNF promoter region". Biochemical and Biophysical Research Communications. 289 (1): 25–33. doi:10.1006/bbrc.2001.5929. PMID 11708771. 
  • Benkoussa M, Brand C, Delmotte MH, Formstecher P, Lefebvre P (July 2002). "Retinoic acid receptors inhibit AP1 activation by regulating extracellular signal-regulated kinase and CBP recruitment to an AP1-responsive promoter". Molecular and Cellular Biology. 22 (13): 4522–34. doi:10.1128/MCB.22.13.4522-4534.2002. PMC 133906 Freely accessible. PMID 12052862. 
  • Santalucía T, Christmann M, Yacoub MH, Brand NJ (September 2003). "Hypertrophic agonists induce the binding of c-Fos to an AP-1 site in cardiac myocytes: implications for the expression of GLUT1". Cardiovascular Research. 59 (3): 639–48. doi:10.1016/S0008-6363(03)00472-3. PMID 14499865. 
  • Beausoleil SA, Jedrychowski M, Schwartz D, Elias JE, Villén J, Li J, Cohn MA, Cantley LC, Gygi SP (August 2004). "Large-scale characterization of HeLa cell nuclear phosphoproteins". Proceedings of the National Academy of Sciences of the United States of America. 101 (33): 12130–5. doi:10.1073/pnas.0404720101. PMC 514446 Freely accessible. PMID 15302935. 
  • Olsen JV, Blagoev B, Gnad F, Macek B, Kumar C, Mortensen P, Mann M (November 2006). "Global, in vivo, and site-specific phosphorylation dynamics in signaling networks". Cell. 127 (3): 635–48. doi:10.1016/j.cell.2006.09.026. PMID 17081983. 

External links

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


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