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Gene Review

FGR  -  FGR proto-oncogene, Src family tyrosine...

Homo sapiens

Synonyms: Gardner-Rasheed feline sarcoma viral (v-fgr) oncogene homolog, Proto-oncogene c-Fgr, SRC2, Tyrosine-protein kinase Fgr, c-fgr, ...
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Disease relevance of FGR

  • Moreover, the same protein was immunoprecipitated from an Epstein-Barr virus-infected Burkitt's lymphoma cell line which expressed c-fgr mRNA but not in its uninfected fgr mRNA-negative counterpart [1].
  • Gardner-Rasheed feline sarcoma viral oncogene homolog (FGR) was the most significant gene to delineate EBV(+)BL [2].
  • Moreover, a 50-fold increase of the steady-state c-fgr mRNA concentration is observed when uninfected Burkitt's lymphoma cell lines are deliberately infected with EBV [3].
  • Recently, we have isolated and characterized the human gene, c-fgr, corresponding to the viral onc sequence and have shown that c-fgr is a unique gene located on the short arm of chromosome 1 (ref. 7). Here we report that certain lymphomas (but not sarcomas or carcinomas) express fgr-related messenger RNA [3].
  • While c-src transcripts were detected in myeloid leukemia cells representative of all stages of differentiation, the highly related gene c-fgr was expressed at high levels only at later developmental stages, both in normal cells committed to the monocytic lineage and in leukemic cells with a differentiated myelomonocytic phenotype [4].

High impact information on FGR


Chemical compound and disease context of FGR


Biological context of FGR

  • Primary structure of the human fgr proto-oncogene product p55c-fgr [1].
  • To verify the deduced amino acid sequence, antibodies were prepared against peptides representing amino- and carboxy-terminal regions of the predicted c-fgr translational product [1].
  • Both antibodies specifically recognized a 55-kilodalton protein expressed in COS-1 cells transfected with a c-fgr cDNA expression plasmid [1].
  • SRC2 potentiated transactivation two- to three-fold while SRC3 potentiated transactivation five- to eight-fold [10].
  • In the case of the mammary gland, whole-mount and histological analyses revealed the absence of significant branching morphogenesis in the hormone-treated PR(Cre/+)SRC-2(flox/flox) mammary gland, reinforcing an important role for mammary SRC-2 in cellular proliferative events that require PR [11].

Anatomical context of FGR

  • The c-fgr proto-oncogene: expression in Epstein-Barr-virus-infected B lymphocytes and in cells of the myelomonocytic and granulocytic lineages [12].
  • The enzyme activity and the expression pattern of p55c-fgr suggest that it is involved in regulating the responses of terminally differentiated granulocytes and monocytes to external stimuli, perhaps by controlling changes in cytoskeletal structure [12].
  • The only normal cells in which the c-fgr gene is known to be expressed are peripheral-blood granulocytes and monocytes, and tissue macrophages [12].
  • This interaction represents a potential mechanism by which T-cell growth may be regulated and offers a model by which other members of the src family (products of c-src, c-yes, c-fgr, etc.) may interact with mammalian growth factor receptors [13].
  • Cycloheximide also caused accumulation of c-fgr transcripts in U937 cells; no superinduction was observed when TPA and cycloheximide were added at the same time [14].

Associations of FGR with chemical compounds

  • The c-fgr proto-oncogene, which is a member of the c-src gene family, encodes the cytoplasmic tyrosine kinase p55c-fgr [12].
  • The expression of c-fgr was preceded by growth arrest of DMSO-treated cells, as determined by [3H]-thymidine incorporation and colony-forming ability, and it became detectable when cells committed for terminal differentiation [15].
  • In contrast, when secondary granule secretion was induced with the chemoattractant peptide, formyl-Met-Leu-Phe, a marked decrease in p55c-fgr and FGR kinase was observed in fractions depleted of secondary granules [16].
  • Definite proof of renin-angiotensin aldosterone system activation in FGR should rely on evaluation of additional patients with massive glucosuria [17].
  • Our findings of normal localization and density of placental IGF-IR in FGR encourage us to extend our work to look at the effects of maternal IGF-I on the transport of glucose and amino acids [18].

Other interactions of FGR

  • Peptide mapping demonstrated that the fyn protein was distinct from the closely related c-src and c-fgr proteins [19].
  • Genetic linkage analysis of the 40 families provided by the Centre d'Etude du Polymorphisme Humain (CEPH) showed that FGR maps to a location 3.1 cM from the Rh blood group locus (RH), and falls in the 17.5-cM gap between alpha-fucosidase (FUCA1) and D1S57 [20].
  • We conclude that either c-fgr or lyn is physically associated with CD24 in a cell-type depending manner [21].
  • Currently, the genetic linkage of FN1 and FGR is unique to cattle and thus localizes a site of chromosomal evolution to a 22-cM interval between the two loci [22].
  • Novel association of the src family kinases, hck and c-fgr, with CCR3 receptor stimulation: A possible mechanism for eotaxin-induced human eosinophil chemotaxis [23].

Analytical, diagnostic and therapeutic context of FGR

  • Further analyses by CGH on microarrays demonstrated a progressively increasing gain of mixed lineage leukemia (MLL) gene (11q23) in U-2OS MTX-resistant variants, which was also confirmed by fluorescence in situ hybridization (FISH), in addition to gain of FGR (1p36), amplification/overexpression of DHFR, and slight decrease of RFC expression [24].
  • Restriction mapping and partial sequence analyses revealed that two of these clones were derived from the c-fgr gene, distinct from the c-yes gene [25].
  • Furthermore, karyotype analysis of several human-mouse hybrid cells and Southern blot analyses of DNAs of the hybrids with a human c-fgr locus-specific probe showed that this gene is located on chromosome 1 [25].
  • Northern blot hybridization analysis using the c-fgr specific sequence showed that the c-fgr mRNA was expressed at higher level in the liver than in the brain, lung, or kidney of a human fetus [26].
  • In twins with discordant weight, RI was increased in the growth restricted (FGR) twin than the appropriate for gestational age (AGA) co-twin (0.46 +/- 0.02 vs 0.3 +/- 0.01; P< 0.001) and the control group (P< 0.001) [27].


  1. Primary structure of the human fgr proto-oncogene product p55c-fgr. Katamine, S., Notario, V., Rao, C.D., Miki, T., Cheah, M.S., Tronick, S.R., Robbins, K.C. Mol. Cell. Biol. (1988) [Pubmed]
  2. Comparison of gene expression profiles of lymphoma cell lines from transformed follicular lymphoma, Burkitt's lymphoma and de novo diffuse large B-cell lymphoma. Maesako, Y., Uchiyama, T., Ohno, H. Cancer Sci. (2003) [Pubmed]
  3. fgr proto-oncogene mRNA induced in B lymphocytes by Epstein-Barr virus infection. Cheah, M.S., Ley, T.J., Tronick, S.R., Robbins, K.C. Nature (1986) [Pubmed]
  4. Differential expression and regulation of the c-src and c-fgr protooncogenes in myelomonocytic cells. Willman, C.L., Stewart, C.C., Griffith, J.K., Stewart, S.J., Tomasi, T.B. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  5. Augmented expression of a myeloid-specific protein tyrosine kinase gene (hck) after macrophage activation. Ziegler, S.F., Wilson, C.B., Perlmutter, R.M. J. Exp. Med. (1988) [Pubmed]
  6. Beta 2 integrin-dependent protein tyrosine phosphorylation and activation of the FGR protein tyrosine kinase in human neutrophils. Berton, G., Fumagalli, L., Laudanna, C., Sorio, C. J. Cell Biol. (1994) [Pubmed]
  7. Expression of the fgr protooncogene product as a function of myelomonocytic cell maturation. Notario, V., Gutkind, J.S., Imaizumi, M., Katamine, S., Robbins, K.C. J. Cell Biol. (1989) [Pubmed]
  8. The murine c-fgr gene product associated with Ly6C and p70 integral membrane protein is expressed in cells of a monocyte/macrophage lineage. Hatakeyama, S., Iwabuchi, K., Ogasawara, K., Good, R.A., Onoé, K. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  9. Retinoic acid induces changes in c-fgr proto-oncogene mRNA levels in Burkitt's lymphoma cells. Faulkner, L., Katz, D.R., Brickell, P.M. Immunobiology (1993) [Pubmed]
  10. Regulation of human estrogen receptor alpha-mediated gene transactivation in Saccharomyces cerevisiae by human coactivator and corepressor proteins. Bitter, G.A. J. Steroid Biochem. Mol. Biol. (2007) [Pubmed]
  11. Steroid receptor coactivator 2 is essential for progesterone-dependent uterine function and mammary morphogenesis: Insights from the mouse-implications for the human. Mukherjee, A., Amato, P., Allred, D.C., Fernandez-Valdivia, R., Nguyen, J., O'malley, B.W., Demayo, F.J., Lydon, J.P. J. Steroid Biochem. Mol. Biol. (2006) [Pubmed]
  12. The c-fgr proto-oncogene: expression in Epstein-Barr-virus-infected B lymphocytes and in cells of the myelomonocytic and granulocytic lineages. Patel, M., Faulkner, L., Katz, D.R., Brickell, P.M. Pathobiology (1991) [Pubmed]
  13. The CD4 and CD8 antigens are coupled to a protein-tyrosine kinase (p56lck) that phosphorylates the CD3 complex. Barber, E.K., Dasgupta, J.D., Schlossman, S.F., Trevillyan, J.M., Rudd, C.E. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  14. Tissue-specific expression and developmental regulation of the human fgr proto-oncogene. Ley, T.J., Connolly, N.L., Katamine, S., Cheah, M.S., Senior, R.M., Robbins, K.C. Mol. Cell. Biol. (1989) [Pubmed]
  15. fgr proto-oncogene is expressed during terminal granulocytic differentiation of human promyelocytic HL60 cells. Miyazaki, Y., Katamine, S., Kohno, T., Moriuchi, R., Miyamoto, T., Tomonaga, M. Exp. Hematol. (1993) [Pubmed]
  16. Translocation of the FGR protein-tyrosine kinase as a consequence of neutrophil activation. Gutkind, J.S., Robbins, K.C. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  17. Familial renal glucosuria: SLC5A2 mutation analysis and evidence of salt-wasting. Calado, J., Loeffler, J., Sakallioglu, O., Gok, F., Lhotta, K., Barata, J., Rueff, J. Kidney Int. (2006) [Pubmed]
  18. An immunohistochemical study of type I insulin-like growth factor receptors in the placentae of pregnancies with appropriately grown or growth restricted fetuses. Holmes, R., Porter, H., Newcomb, P., Holly, J.M., Soothill, P. Placenta (1999) [Pubmed]
  19. In vivo phosphorylation and membrane association of the fyn proto-oncogene product in IM-9 human lymphoblasts. Peters, D.J., McGrew, B.R., Perron, D.C., Liptak, L.M., Laudano, A.P. Oncogene (1990) [Pubmed]
  20. Localization of the FGR protooncogene on the genetic linkage map of human chromosome 1p. Dracopoli, N.C., Stanger, B.Z., Lager, M., Housman, D.E. Genomics (1988) [Pubmed]
  21. Association of CD24 with the kinase c-fgr in a small cell lung cancer cell line and with the kinase lyn in an erythroleukemia cell line. Zarn, J.A., Zimmermann, S.M., Pass, M.K., Waibel, R., Stahel, R.A. Biochem. Biophys. Res. Commun. (1996) [Pubmed]
  22. A genetic map of nine loci on bovine chromosome 2. Beever, J.E., Da, Y., Ron, M., Lewin, H.A. Mamm. Genome (1994) [Pubmed]
  23. Novel association of the src family kinases, hck and c-fgr, with CCR3 receptor stimulation: A possible mechanism for eotaxin-induced human eosinophil chemotaxis. El-Shazly, A., Yamaguchi, N., Masuyama, K., Suda, T., Ishikawa, T. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
  24. Genomic imbalances associated with methotrexate resistance in human osteosarcoma cell lines detected by comparative genomic hybridization-based techniques. Hattinger, C.M., Reverter-Branchat, G., Remondini, D., Castellani, G.C., Benini, S., Pasello, M., Manara, M.C., Scotlandi, K., Picci, P., Serra, M. Eur. J. Cell Biol. (2003) [Pubmed]
  25. Structure, expression, and chromosomal location of the human c-fgr gene. Nishizawa, M., Semba, K., Yoshida, M.C., Yamamoto, T., Sasaki, M., Toyoshima, K. Mol. Cell. Biol. (1986) [Pubmed]
  26. Isolation and sequencing of cDNA clones homologous to the v-fgr oncogene from a human B lymphocyte cell line, IM-9. Inoue, K., Ikawa, S., Semba, K., Sukegawa, J., Yamamoto, T., Toyoshima, K. Oncogene (1987) [Pubmed]
  27. Non-invasive method of evaluation of trophoblast invasion of spiral arteries in monochorionic twins with discordant birthweight. Matijevic, R., Ward, S., Bajoria, R. Placenta (2002) [Pubmed]
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