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Fgf3

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Fgf3

Fibroblast growth factor 3
Identifiers
Symbols  ; HBGF-3; INT2
External IDs GeneCards:
RNA expression pattern
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)
PubMed search

INT-2 proto-oncogene protein also known as FGF-3 is a protein that in humans is encoded by the FGF3 gene.[1]

Contents

  • Function 1
  • Clinical significance 2
  • Interactions 3
  • References 4
  • Further reading 5

Function

FGF-3 is a member of the fibroblast growth factor family. FGF3 binds to Fibroblast Growth Factor Receptor 3 (FGFR3) to serve as a negative regulator of bone growth during ossification. Effectively, FGF-3 inhibits proliferation of chondrocytes within growth plate.

FGF family members possess broad mitogenic and cell survival activities and are involved in a variety of biological processes including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion.[1]

Clinical significance

The FGF3 gene was identified by its similarity with mouse fgf3/int-2, a proto-oncogene activated in virally induced mammary tumors in the mouse. Frequent amplification of this gene has been found in human tumors, which may be important for neoplastic transformation and tumor progression. Studies of the similar genes in mouse and chicken suggested the role in inner ear formation.[1] Also, haploinsufficiency in the FGF3 gene is thought to cause otodental syndrome.

Interactions

FGF3 (gene) has been shown to interact with EBNA1BP2.[2]

References

  1. ^ a b c "Entrez Gene: FGF3 fibroblast growth factor 3 (murine mammary tumor virus integration site (v-int-2) oncogene homolog)". 
  2. ^ Reimers, K; Antoine M; Zapatka M; Blecken V; Dickson C; Kiefer P (Aug 2001). "NoBP, a nuclear fibroblast growth factor 3 binding protein, is cell cycle regulated and promotes cell growth". Mol. Cell. Biol. (United States) 21 (15): 4996–5007.  

Further reading

  • Represa J, León Y, Miner C, Giraldez F (1991). "The int-2 proto-oncogene is responsible for induction of the inner ear.". Nature 353 (6344): 561–3.  
  • Brookes S, Smith R, Casey G, et al. (1989). "Sequence organization of the human int-2 gene and its expression in teratocarcinoma cells.". Oncogene 4 (4): 429–36.  
  • Casey G, Smith R, McGillivray D, et al. (1987). "Characterization and chromosome assignment of the human homolog of int-2, a potential proto-oncogene.". Mol. Cell. Biol. 6 (2): 502–10.  
  • Mansour SL, Goddard JM, Capecchi MR (1993). "Mice homozygous for a targeted disruption of the proto-oncogene int-2 have developmental defects in the tail and inner ear.". Development 117 (1): 13–28.  
  • Ornitz DM, Xu J, Colvin JS, et al. (1996). "Receptor specificity of the fibroblast growth factor family.". J. Biol. Chem. 271 (25): 15292–7.  
  • Galdemard C, Yamagata H, Brison O, Lavialle C (2000). "Regulation of FGF-3 gene expression in tumorigenic and non-tumorigenic clones of a human colon carcinoma cell line.". J. Biol. Chem. 275 (23): 17364–73.  
  • Reimers K, Antoine M, Zapatka M, et al. (2001). "NoBP, a nuclear fibroblast growth factor 3 binding protein, is cell cycle regulated and promotes cell growth.". Mol. Cell. Biol. 21 (15): 4996–5007.  
  • 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.  
  • Popovici C, Conchonaud F, Birnbaum D, Roubin R (2004). "Functional phylogeny relates LET-756 to fibroblast growth factor 9.". J. Biol. Chem. 279 (38): 40146–52.  
  • 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.  
  • Antoine M, Reimers K, Wirz W, et al. (2006). "Fibroblast growth factor 3, a protein with a dual subcellular fate, is interacting with human ribosomal protein S2.". Biochem. Biophys. Res. Commun. 338 (2): 1248–55.  
  • Tekin M, Hişmi BO, Fitoz S, et al. (2007). "Homozygous mutations in fibroblast growth factor 3 are associated with a new form of syndromic deafness characterized by inner ear agenesis, microtia, and microdontia.". Am. J. Hum. Genet. 80 (2): 338–44.  
  • Riley BM, Mansilla MA, Ma J, et al. (2007). "Impaired FGF signaling contributes to cleft lip and palate.". Proc. Natl. Acad. Sci. U.S.A. 104 (11): 4512–7.  




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