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Home All issues Volume 20 / No 6-7 (Juin-Juillet 2004) Med Sci (Paris), 20 6-7 (2004) 617-619 References
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Issue
Med Sci (Paris)
Volume 20, Number 6-7, Juin-Juillet 2004
Page(s) 617 - 619
Section Le Magazine : Nouvelles
DOI https://doi.org/10.1051/medsci/2004206-7617
Published online 15 June 2004
  1. Abdelhak, S., Kalatzis V, Heilig R, et al. A human homologue of the Drosophila eyes absent gene underlies branchio-oto-renal (BOR) syndrome and identifies a novel gene family. Nat Genet 1997; 15 : 157–64. [Google Scholar]
  2. Vincent C, Kalatzis V, Abdelhak S, et al. BOR and BO syndromes are allelic defects of EYA1. Eur J Hum Genet 1997; 5 : 242–6. [Google Scholar]
  3. Wayne S, Robertson NG, DeClau F, et al. Mutations in the transcriptional activator EYA4 cause late-onset deafness at the DFNA10 locus. Hum Mol Genet 2001; 10 : 195–200. [Google Scholar]
  4. Xu PX, Adams J, Peters H, et al. Eya1-deficient mice lack ears and kidneys and show abnormal apoptosis of organ primordia. Nat Genet 1999; 23 : 113–7. [Google Scholar]
  5. Xu PX, Zheng W, Laclef C, et al. Eya1 is required for the morphogenesis of mammalian thymus, parathyroid and thyroid. Development 2002; 129 : 3033–44. [Google Scholar]
  6. Wawersik S, Maas RL. Vertebrate eye development as modeled in Drosophila. Hum Mol Genet 2000; 9 : 917–25. [Google Scholar]
  7. Heanue TA, Reshef R, Davis RJ, et al. Synergistic regulation of vertebrate muscle development by Dach2, Eya2, and Six1, homologs of genes required for Drosophila eye formation. Genes Dev 1999;13 : 3231–43. [Google Scholar]
  8. Ohto H, Kamada S, Tago K, et al. Cooperation of six and eya in activation of their target genes through nuclear translocation of Eya. Mol Cell Biol 1999; 19 : 6815–24. [Google Scholar]
  9. Li X, Perissi V, Liu F, et al. Tissue-specific regulation of retinal and pituitary precursor cell proliferation. Science 2002; 297 : 1180–3. [Google Scholar]
  10. Li X, Oghi KA, Zhang J, et al. Eya protein phosphatase activity regulates Six1-Dach-Eya transcriptional effects in mammalian organogenesis. Nature 2003; 426 : 247–54. [Google Scholar]
  11. Ikeda K, Watanabe Y, Ohto H, Kawakami K. Molecular interaction and synergistic activation of a promoter by Six, Eya, and Dach proteins mediated through CREB binding protein. Mol Cell Biol 2002; 22 : 6759–66. [Google Scholar]
  12. Fan X, Brass LF, Poncz M, et al. The alpha subunits of Gz and Gi interact with the eyes absent transcription cofactor Eya2, preventing its interaction with the six class of homeodomain-containing proteins. J Biol Chem 2000; 275 : 32129–34. [Google Scholar]
  13. Rayapureddi JP, Kattamuri C, Steinmetz BD, et al. Eyes absent represents a class of protein tyrosine phosphatases. Nature 2003; 426 : 295–8. [Google Scholar]
  14. Tootle TL, Silver SJ, Davies EL, et al. The transcription factor Eyes absent is a protein tyrosine phosphatase. Nature 2003; 426 : 299–302. [Google Scholar]
  15. Silver SJ, Davies EL, Doyon L, Rebay I. Functional dissection of eyes absent reveals new modes of regulation within the retinal determination gene network. Mol Cell Biol 2003; 23 : 5989–99. [Google Scholar]
  16. Ozaki H, Watanabe Y, Ikeda K, Kawakami K. Impaired interactions between mouse Eyal harboring mutations found in patients with branchio-oto-renal syndrome and Six, Dach, and G proteins. J Hum Genet 2002; 47 : 107–16. [Google Scholar]

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