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Gene Review

FES  -  FES proto-oncogene, tyrosine kinase

Homo sapiens

Synonyms: FPS, Feline sarcoma/Fujinami avian sarcoma oncogene homolog, Proto-oncogene c-Fes, Proto-oncogene c-Fps, Tyrosine-protein kinase Fes/Fps, ...
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Disease relevance of FES


Psychiatry related information on FES

  • This paper aimed to examine the relationship between the trichotomous symptom structure of psychopathology and neuropsychological functioning in young people with first episode schizophrenia (FES), most of whom were receiving atypical antipsychotic medication [6].
  • Finally, correlation analyses showed that for FES participants both executive and language tests significantly correlated with ANWLG total responses, while the correlation between ANWLG and only 1 language test was significant for LTLE participants [7].
  • Forty-three adolescents with anorexia nervosa and 85 controls were administered the EAT, EDI, and FES [8].
  • A total of 316 adolescents completed the self-administered questionnaire: The DSD, Somatic Symptom Scale, SAFE-C, FES, Coping, and Rosenberg's Self-Esteem Scale [9].
  • Although ample research has documented the utility of the FES in predicting important cognitive and behavioral outcomes, psychometric data on the scale are lacking [10].

High impact information on FES

  • Expression of the 93-kd tyrosine kinase encoded by the human c-fes proto-oncogene (also known as FES) is restricted to mature hematopoietic cells of the granulocytic and monocytic lineages, suggestive of a function essential to normal myeloid differentiation [11].
  • Therefore, BLM, the gene that when mutated gives rise to Bloom syndrome, is tightly linked to FES, a gene whose chromosome position is known to be 15q26 [12].
  • The locus mutated in BS, BLM, maps to chromosome subband 15q26.1, tightly linked to the proto-oncogene FES [13].
  • A striking association of the C3 allele at FES with blm (delta = .422; p = 5.52 x 10(-7)) and of the 145-bp and 147-bp alleles at D15S127 with blm (delta = .392 and delta = .483, respectively; p = 2.8 x 10(-5) and p = 5.4 x 10(-7), respectively) was detected in Ashkenazi Jews with BS [13].
  • We demonstrate herein that IL-4 stimulation induced rapid association of FES or a related protein with PI3 kinase in mouse T-cell lines [14].

Chemical compound and disease context of FES


Biological context of FES


Anatomical context of FES


Associations of FES with chemical compounds

  • Furthermore, tyrosine phosphorylated FES or the closely related protein is found associated with the IL-4R [25].
  • This result, along with the prior assignment of the loci for mitochondrial isocitrate dehydrogenase and FES to human chromosome 15 and mouse chromosome 7, suggest a conserved autosomal synteny group on the distal long arm of HSA15 and in the center of MMU7 [26].
  • This linkage disequilibrium constitutes strong support for a founder-effect hypothesis: the chromosome in the hypothetical founder who carried blm also carried the C3 allele at FES and either the 145-bp or the 147-bp allele at D15S127 [13].
  • We also wanted to establish the dose level of the anti-estrogen tamoxifen required to block target tissue uptake of FES [27].
  • We have measured in vivo the uptake of 16 alpha-[18F]estradiol (FES) by target tissues in the immature rat at increasing dose levels (obtained by dilution of [18F]FES with unlabeled estradiol) [27].
  • FES is phosphorylated on tyrosine residues in cells that carry KIT(D816V) mutation, and this phosphorylation is KIT dependent [28].

Physical interactions of FES

  • Through a deletion analysis of the IL-4R we have identified a putative FES-binding site in the cytoplasmic domain of the IL-4R [25].

Regulatory relationships of FES

  • The FER gene is evolutionarily conserved and encodes a widely expressed member of the FPS/FES protein-tyrosine kinase family [29].

Other interactions of FES

  • Previous work in our laboratory has established that BCR is a substrate for c-FES, a non-receptor tyrosine kinase linked to myeloid growth and differentiation [19].
  • The relationship between her genotype and phenotype are discussed in light of genes, including IGF1R and FES, mapped to the aneusomic segment [30].
  • FES at 15q26.1 is also distal to the breakpoint in chromosome 15 in the translocation commonly seen in acute promyelocytic leukemia, t(15;17) (q24;q22) [3].
  • LOMs (STRs: CD4, FES, F13B, TH01) are characterised by a number of repeats between 5-15 and a stable repeat sequence [31].
  • Comparing the genomic structure of CSK with the exon/intron organisation of both, it is obvious that the exon/intron boundaries are in common either with those of the SRC-type or the FES boundaries [32].

Analytical, diagnostic and therapeutic context of FES

  • Confirmation of 15q26.1 as the site of the FES protooncogene by fluorescence in situ hybridization [22].
  • Forty-one patients with FES and 47 matched healthy controls underwent a T1-weighted structural MRI scan [23].
  • Detrusor activity was inhibited by FES (functional electrical stimulation) applied to the anal sphincter causing decreased bladder spasticity and increased bladder capacity [33].
  • Data on the incomes of families with a severely disabled child were obtained by replicating the Family Expenditure Survey. These data were compared with income data from a control group of families with children, drawn from the FES for the same period [34].
  • Effects of joint motion constraints on the gait of normal subjects and their implications on the further development of hybrid FES orthosis for paraplegic persons [35].


  1. Human c-FES is a nuclear tyrosine kinase. Yates, K.E., Lynch, M.R., Wong, S.G., Slamon, D.J., Gasson, J.C. Oncogene (1995) [Pubmed]
  2. Abnormal protein tyrosine kinase gene expression during melanoma progression and metastasis. Easty, D.J., Herlyn, M., Bennett, D.C. Int. J. Cancer (1995) [Pubmed]
  3. Localization of the cellular oncogenes ABL, SIS, and FES on human germ-line chromosomes. Jhanwar, S.C., Neel, B.G., Hayward, W.S., Chaganti, R.S. Cytogenet. Cell Genet. (1984) [Pubmed]
  4. DNA copy number changes and evaluation of MYC, IGF1R, and FES amplification in xenografts of pancreatic adenocarcinoma. Armengol, G., Knuutila, S., Lluís, F., Capellà, G., Miró, R., Caballín, M.R. Cancer Genet. Cytogenet. (2000) [Pubmed]
  5. 16 beta-([18F]fluoro)estrogens: systematic investigation of a new series of fluorine-18-labeled estrogens as potential imaging agents for estrogen-receptor-positive breast tumors. VanBrocklin, H.F., Carlson, K.E., Katzenellenbogen, J.A., Welch, M.J. J. Med. Chem. (1993) [Pubmed]
  6. Neuropsychological correlates of symptom profiles in first episode schizophrenia. Lucas, S., Fitzgerald, D., Redoblado-Hodge, M.A., Anderson, J., Sanbrook, M., Harris, A., Brennan, J. Schizophr. Res. (2004) [Pubmed]
  7. Category fluency in first-episode schizophrenia. Giovannetti, T., Goldstein, R.Z., Schullery, M., Barr, W.B., Bilder, R.M. Journal of the International Neuropsychological Society : JINS. (2003) [Pubmed]
  8. Testing the hypothesis of the multidimensional model of anorexia nervosa in adolescents. Lyon, M., Chatoor, I., Atkins, D., Silber, T., Mosimann, J., Gray, J. Adolescence. (1997) [Pubmed]
  9. Ethnic differences in adolescents' mental distress, social stress, and resources. Choi, H., Meininger, J.C., Roberts, R.E. Adolescence. (2006) [Pubmed]
  10. Perceived likelihood as a measure of optimism and pessimism: support for the Future Events Scale. Wichman, A.L., Reich, D.A., Weary, G. Psychological assessment. (2006) [Pubmed]
  11. Elevated expression of the c-fes proto-oncogene in adult human myeloid leukemia cells in the absence of gene amplification. Smithgall, T.E., Johnston, J.B., Bustin, M., Glazer, R.I. J. Natl. Cancer Inst. (1991) [Pubmed]
  12. Bloom syndrome: an analysis of consanguineous families assigns the locus mutated to chromosome band 15q26.1. German, J., Roe, A.M., Leppert, M.F., Ellis, N.A. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  13. Linkage disequilibrium between the FES, D15S127, and BLM loci in Ashkenazi Jews with Bloom syndrome. Ellis, N.A., Roe, A.M., Kozloski, J., Proytcheva, M., Falk, C., German, J. Am. J. Hum. Genet. (1994) [Pubmed]
  14. Interleukin-4 induces association of the c-fes proto-oncogene product with phosphatidylinositol-3 kinase. Izuhara, K., Feldman, R.A., Greer, P., Harada, N. Blood (1996) [Pubmed]
  15. Positron tomographic assessment of 16 alpha-[18F] fluoro-17 beta-estradiol uptake in metastatic breast carcinoma. McGuire, A.H., Dehdashti, F., Siegel, B.A., Lyss, A.P., Brodack, J.W., Mathias, C.J., Mintun, M.A., Katzenellenbogen, J.A., Welch, M.J. J. Nucl. Med. (1991) [Pubmed]
  16. Positron emission tomographic assessment of "metabolic flare" to predict response of metastatic breast cancer to antiestrogen therapy. Dehdashti, F., Flanagan, F.L., Mortimer, J.E., Katzenellenbogen, J.A., Welch, M.J., Siegel, B.A. European journal of nuclear medicine. (1999) [Pubmed]
  17. Physiologic effects of electrical stimulation leg cycle exercise training in spinal cord injured persons. Hooker, S.P., Figoni, S.F., Rodgers, M.M., Glaser, R.M., Mathews, T., Suryaprasad, A.G., Gupta, S.C. Archives of physical medicine and rehabilitation. (1992) [Pubmed]
  18. Electrical stimulation of abdominal muscles for control of blood pressure and augmentation of cough in a C3/4 level tetraplegic. Taylor, P.N., Tromans, A.M., Harris, K.R., Swain, I.D. Spinal Cord (2002) [Pubmed]
  19. Co-expression with BCR induces activation of the FES tyrosine kinase and phosphorylation of specific N-terminal BCR tyrosine residues. Li, J., Smithgall, T.E. J. Biol. Chem. (1996) [Pubmed]
  20. Tetranucleotide repeat polymorphism at the human c-fes/fps proto-oncogene (FES). Polymeropoulos, M.H., Rath, D.S., Xiao, H., Merril, C.R. Nucleic Acids Res. (1991) [Pubmed]
  21. Comparative mapping of IGHG1, IGHM, FES, and FOS in domestic cattle. Tobin-Janzen, T.C., Womack, J.E. Immunogenetics (1992) [Pubmed]
  22. Confirmation of 15q26.1 as the site of the FES protooncogene by fluorescence in situ hybridization. Mathew, S., Murty, V.V., German, J., Chaganti, R.S. Cytogenet. Cell Genet. (1993) [Pubmed]
  23. Progressive grey matter atrophy over the first 2-3 years of illness in first-episode schizophrenia: a tensor-based morphometry study. Whitford, T.J., Grieve, S.M., Farrow, T.F., Gomes, L., Brennan, J., Harris, A.W., Gordon, E., Williams, L.M. Neuroimage (2006) [Pubmed]
  24. Elastosis and fragmentation of fibers of the elastic system in fatal asthma. Mauad, T., Xavier, A.C., Saldiva, P.H., Dolhnikoff, M. Am. J. Respir. Crit. Care Med. (1999) [Pubmed]
  25. Interaction of the c-fes proto-oncogene product with the interleukin-4 receptor. Izuhara, K., Feldman, R.A., Greer, P., Harada, N. J. Biol. Chem. (1994) [Pubmed]
  26. Insulin-like growth factor I receptor gene is concordant with c-Fes protooncogene and mouse chromosome 7 in somatic cell hybrids. Sundaresan, S., Francke, U. Somat. Cell Mol. Genet. (1989) [Pubmed]
  27. Titration of the in vivo uptake of 16 alpha-[18F]fluoroestradiol by target tissues in the rat: competition by tamoxifen, and implications for quantitating estrogen receptors in vivo and the use of animal models in receptor-binding radiopharmaceutical development. Katzenellenbogen, J.A., Mathias, C.J., VanBrocklin, H.F., Brodack, J.W., Welch, M.J. Nucl. Med. Biol. (1993) [Pubmed]
  28. The tyrosine kinase FES is an essential effector of KITD816V proliferation signal. Voisset, E., Lopez, S., Dubreuil, P., De Sepulveda, P. Blood (2007) [Pubmed]
  29. The FER gene is evolutionarily conserved and encodes a widely expressed member of the FPS/FES protein-tyrosine kinase family. Pawson, T., Letwin, K., Lee, T., Hao, Q.L., Heisterkamp, N., Groffen, J. Mol. Cell. Biol. (1989) [Pubmed]
  30. Tetrasomy 15q25.3 --> qter resulting from an analphoid supernumerary marker chromosome in a patient with multiple anomalies and bilateral Wilms tumors. Hu, J., McPherson, E., Surti, U., Hasegawa, S.L., Gunawardena, S., Gollin, S.M. Am. J. Med. Genet. (2002) [Pubmed]
  31. Population genetic diversity in relation to microsatellite heterogeneity. Brinkmann, B., Junge, A., Meyer, E., Wiegand, P. Hum. Mutat. (1998) [Pubmed]
  32. Characterization of the human CSK locus. Bräuninger, A., Karn, T., Strebhardt, K., Rübsamen-Waigmann, H. Oncogene (1993) [Pubmed]
  33. Bladder inhibition with functional electrical stimulation. Godec, C., Cass, A.S., Ayala, G.F. Urology (1975) [Pubmed]
  34. Childhood disablement and family incomes. Baldwin, S., Godfrey, C., Staden, F. Journal of epidemiology and community health. (1983) [Pubmed]
  35. Effects of joint motion constraints on the gait of normal subjects and their implications on the further development of hybrid FES orthosis for paraplegic persons. Yang, L., Condie, D.N., Granat, M.H., Paul, J.P., Rowley, D.I. Journal of biomechanics. (1996) [Pubmed]
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