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Gene Review

Fgfr4  -  fibroblast growth factor receptor 4

Mus musculus

Synonyms: FGFR-4, Fgfr-4, Fibroblast growth factor receptor 4, Mpk-11, Protein-tyrosine kinase receptor MPK-11
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Disease relevance of Fgfr4

  • However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities [1].
  • To determine whether FGFR4 expression regulates myoblast differentiation, we infected a soluble dominant-negative FGFR4-containing adenovirus into these cells [2].
  • Chronic CCl(4) exposure resulted in severe fibrosis in livers of FGFR4-deficient mice compared to normal mice [3].
  • To validate this model in primary human pituitary tumors, we examined the expression of ptd-FGFR4, N-cadherin, and clinical behavior [4].

High impact information on Fgfr4

  • 1. Furthermore, the temporal expression and selective inhibition of FGF receptors 1 and 4 present within the endoderm implies that signaling through FGFR4 is involved in specifying lung versus liver [5].
  • An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels [1].
  • FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung [1].
  • Fgfr4 is a putative receptor for FGF6 [6].
  • These results suggest that FGFR-4 is likely to have diverse roles in development, which may include regulation of definitive endoderm and skeletal muscle lineages [7].

Chemical compound and disease context of Fgfr4


Biological context of Fgfr4

  • Responsiveness of developing dental tissues to fibroblast growth factors: expression of splicing alternatives of FGFR1, -2, -3, and of FGFR4; and stimulation of cell proliferation by FGF-2, -4, -8, and -9 [8].
  • These results suggest that FGFR4 may be an important regulator of osteogenesis with involvement in preosteoblast proliferation and differentiation as well as osteoblast functioning during intramembranous ossification [9].
  • To begin to dissect the molecular pathways involving Fgfr4, we queried the promoter sequences for transcriptional factor binding sites and tested candidate regulators in a 27-time point regeneration series [10].
  • Fgfr4 has been shown to be important for appropriate muscle development in chick limb buds; however, Fgfr4 null mice show no phenotype [10].
  • FGFR1, FGFR2, and FGFR4 have unique patterns of expression during embryogenesis suggesting that these receptors mediate different functions of FGFs during development [11].

Anatomical context of Fgfr4

  • FGFR-4 protein was detected in all cells of the implanting embryo, but was restricted to the ICM/primitive endoderm in later stage outgrowths [12].
  • We tested blastocyst outgrowths, a model for implantation, for FGFR-3 and FGFR-4 protein [12].
  • Immunocytochemical analysis of primary osteoblast cultures taken from the same cranial region also revealed high levels of FGFR4 expression, suggesting a similar pattern of cellular expression in vivo and in vitro [9].
  • We have investigated the expression pattern of FGFR4 in the neonatal mouse calvaria and compared it to the expression pattern in cultures of primary osteoblasts [9].
  • Our findings point to distinct transcriptional regulation and action for FGFR4 in differentiating skeletal muscle cells [2].

Associations of Fgfr4 with chemical compounds

  • The results demonstrate that transmembrane sensors interface with metabolite-controlled transcription networks and suggest that pericellular matrix-controlled liver FGFR4 in particular may ensure adequate cholesterol for cell structures and signal transduction [13].
  • Mutation of tyrosine Y754F in ptd-FGFR4 abrogated the effect of PD173074-mediated inhibition [4].
  • One of these regions is within the kinase domain's activation loop, where FGFR-1, but not FGFR-4, bears a key aspartate residue [14].
  • Targeting N-Cadherin through Fibroblast Growth Factor Receptor-4: Distinct Pathogenetic and Therapeutic Implications [4].

Regulatory relationships of Fgfr4


Other interactions of Fgfr4


Analytical, diagnostic and therapeutic context of Fgfr4


  1. FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung. Weinstein, M., Xu, X., Ohyama, K., Deng, C.X. Development (1998) [Pubmed]
  2. Distinct transcriptional control and action of fibroblast growth factor receptor 4 in differentiating skeletal muscle cells. Yu, S., Zheng, L., Trinh, D.K., Asa, S.L., Ezzat, S. Lab. Invest. (2004) [Pubmed]
  3. Increased carbon tetrachloride-induced liver injury and fibrosis in FGFR4-deficient mice. Yu, C., Wang, F., Jin, C., Wu, X., Chan, W.K., McKeehan, W.L. Am. J. Pathol. (2002) [Pubmed]
  4. Targeting N-Cadherin through Fibroblast Growth Factor Receptor-4: Distinct Pathogenetic and Therapeutic Implications. Ezzat, S., Zheng, L., Winer, D., Asa, S.L. Mol. Endocrinol. (2006) [Pubmed]
  5. Different thresholds of fibroblast growth factors pattern the ventral foregut into liver and lung. Serls, A.E., Doherty, S., Parvatiyar, P., Wells, J.M., Deutsch, G.H. Development (2005) [Pubmed]
  6. Expression of the Fgf6 gene is restricted to developing skeletal muscle in the mouse embryo. deLapeyrière, O., Ollendorff, V., Planche, J., Ott, M.O., Pizette, S., Coulier, F., Birnbaum, D. Development (1993) [Pubmed]
  7. FGFR-4, a new member of the fibroblast growth factor receptor family, expressed in the definitive endoderm and skeletal muscle lineages of the mouse. Stark, K.L., McMahon, J.A., McMahon, A.P. Development (1991) [Pubmed]
  8. Responsiveness of developing dental tissues to fibroblast growth factors: expression of splicing alternatives of FGFR1, -2, -3, and of FGFR4; and stimulation of cell proliferation by FGF-2, -4, -8, and -9. Kettunen, P., Karavanova, I., Thesleff, I. Dev. Genet. (1998) [Pubmed]
  9. Fibroblast growth factor receptor 4 (FGFR4) expression in newborn murine calvaria and primary osteoblast cultures. Cool, S., Jackson, R., Pincus, P., Dickinson, I., Nurcombe, V. Int. J. Dev. Biol. (2002) [Pubmed]
  10. Fgfr4 is required for effective muscle regeneration in vivo. Delineation of a MyoD-Tead2-Fgfr4 transcriptional pathway. Zhao, P., Caretti, G., Mitchell, S., McKeehan, W.L., Boskey, A.L., Pachman, L.M., Sartorelli, V., Hoffman, E.P. J. Biol. Chem. (2006) [Pubmed]
  11. Unique expression pattern of the FGF receptor 3 gene during mouse organogenesis. Peters, K., Ornitz, D., Werner, S., Williams, L. Dev. Biol. (1993) [Pubmed]
  12. Expression of fibroblast growth factor receptors in peri-implantation mouse embryos. Rappolee, D.A., Patel, Y., Jacobson, K. Mol. Reprod. Dev. (1998) [Pubmed]
  13. Elevated cholesterol metabolism and bile acid synthesis in mice lacking membrane tyrosine kinase receptor FGFR4. Yu, C., Wang, F., Kan, M., Jin, C., Jones, R.B., Weinstein, M., Deng, C.X., McKeehan, W.L. J. Biol. Chem. (2000) [Pubmed]
  14. Amino acid residues which distinguish the mitogenic potentials of two FGF receptors. Wang, J.K., Goldfarb, M. Oncogene (1997) [Pubmed]
  15. Overlapping expression and redundant activation of mesenchymal fibroblast growth factor (FGF) receptors by alternatively spliced FGF-8 ligands. Blunt, A.G., Lawshé, A., Cunningham, M.L., Seto, M.L., Ornitz, D.M., MacArthur, C.A. J. Biol. Chem. (1997) [Pubmed]
  16. Signal transduction by fibroblast growth factor receptor-4 (FGFR-4). Comparison with FGFR-1. Vainikka, S., Joukov, V., Wennström, S., Bergman, M., Pelicci, P.G., Alitalo, K. J. Biol. Chem. (1994) [Pubmed]
  17. FGF-8 isoforms activate receptor splice forms that are expressed in mesenchymal regions of mouse development. MacArthur, C.A., Lawshé, A., Xu, J., Santos-Ocampo, S., Heikinheimo, M., Chellaiah, A.T., Ornitz, D.M. Development (1995) [Pubmed]
  18. In vivo expression and localization of the fibroblast growth factor system in the intact and lesioned rat peripheral nerve and spinal ganglia. Grothe, C., Meisinger, C., Claus, P. J. Comp. Neurol. (2001) [Pubmed]
  19. Fibroblast growth factor receptor (FGFR)-4, but not FGFR-3 is expressed in the pregnant ovary. Puscheck, E.E., Patel, Y., Rappolee, D.A. Mol. Cell. Endocrinol. (1997) [Pubmed]
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