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VOL. 74 (2), 203-228, 2008  UNA APROXIMACIÓN FARMACOLÓGICA...

(14)  WEBSTER, M. K. and DONOGHUE, D. J. (1996): Constitutive activation of fibro-
(15)  blast growth factor receptor 3 by the transmembrane domain point mutation
(16)  found in achondroplasia. EMBO J. 15: 520-527.
(17)  SOROKIN, A.; LEMMON, M. A.; ULLRICH, A. and SCHLESSINGER, J. (1994): Stabi-
(18)  lization of an active dimeric form of the epidermal growth factor receptor
(19)  by introduction of an inter-receptor disulfide bond. J. Biol. Chem. 269:
(20)  9752-9759.
(21)  LIEVENS, P. M.; MUTINELLI, C.; BAYNES, D. and LIBOI, E. (2004): The kinase
(22)  activity of fibroblast growth factor receptor 3 with activation loop mutations
(23)  affects receptor trafficking and signaling. J. Biol. Chem. 279: 43254-43260.
(24)  CHO, J. Y.; GUO, C.; TORELLO, M.; LUNSTRUM, G. P.; IWATA, T.; DENG, C. and
(25)  HORTON, W. A. (2004): Defective lysosomal targeting of activated fibroblast
(26)  growth factor receptor 3 in achondroplasia. Proc. Natl. Acad. Sci. U.S.A. 101:
      609-614.
      SAHNI, M.; AMBROSETTI, D. C.; MANSUKHANI, A.; GERTNER, R.; LEVY, D. and BA-
      SILICO, C. (1999): FGF signaling inhibits chondrocyte proliferation and regu-
      lates bone development through the STAT-1 pathway. Genes Dev. 13: 1361-
      1366.
      MININA, E.; KRESCHEL, C.; NASKI, M. C.; ORNITZ, D. M. and VORTKAMP, A. (2002):
      Interaction of FGF, Ihh/Pthlh, and BMP signaling integrates chondrocyte
      proliferation and hypertrophic differentiation. Dev. Cell. 3: 439-449.
      DAILEY, L.; LAPLANTINE, E.; PRIORE, R. and BASILICO, C. (2003): A network of
      transcriptional and signaling events is activated by FGF to induce chondro-
      cyte growth arrest and differentiation. J. Cell. Biol. 161: 1053-1066.
      MURAKAMI, S.; BALMES, G.; MCKINNEY, S.; ZHANG, Z.; GIVOL, D. and DE CROM-
      BRUGGHE, B. (2004): Constitutive activation of MEK1 in chondrocytes causes
      Stat1-independent achondroplasia-like dwarfism and rescues the Fgfr3-defi-
      cient mouse phenotype. Genes Dev. 18: 290-305.
      YASODA, A.; KOMATSU, Y.; CHUSHO, H.; MIYAZAWA, T.; OZASA, A.; MIURA, M.; KU-
      RIHARA, T.; ROGI, T.; TANAKA, S.; SUDA, M.; TAMURA, N.; OGAWA, Y. and NAKAO,
      K. (2004): Overexpression of CNP in chondrocytes rescues achondroplasia
      through a MAPK-dependent pathway. Nat. Med. 10: 80-86.
      WANG, Y.; SPATZ, M. K.; KANNAN, K.; HAYK, H.; AVIVI, A.; GORIVODSKY, M.; PINES,
      M.; YAYON, A.; LONAI, P and GIVOL, D. (1999): A mouse model for achondro-
      plasia produced by targeting fibroblast growth factor receptor 3. Proc. Natl.
      Acad. Sci. U. S. A. 96: 4455-4460.
      SEGEV, O.; CHUMAKOV, I.; NEVO, Z.; GIVOL, D.; MADAR-SHAPIRO, L.; SHEININ, Y.;
      WEINREB, M. and YAYON, A. (2000): Restrained chondrocyte proliferation and
      maturation with abnormal growth plate vascularization and ossification in
      human FGFR-3(G380R) transgenic mice. Hum. Mol. Genet. 9: 249-258.
      ROZENBLATT-ROSEN, O.; MOSONEGO-ORNAN, E.; SADOT, E.; MADAR-SHAPIRO, L.; SHEI-
      NIN, Y.; GINSBERG, D. and YAYON, A. (2002): Induction of chondrocyte growth
      arrest by FGF: transcriptional and cytoskeletal alterations. J. Cell. Sci. 115:
      553-562.
      MONSONEGO-ORNAN, E.; ADAR, R.; FEFERMAN, T.; SEGEV, O. and YAYON, A. (2000):
      The transmembrane mutation G380R in fibroblast growth factor receptor 3

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