Reply: role of the dHAND-UFD1L pathway

نویسندگان

  • Srivastava
  • Yamagishi
چکیده

TIG July 1999, volume 15, No. 7 253 cardiac gene expression. J. Mol. Cell. Cardiol. 30, 1673–1681 22 Kleinjan, D-J. and Van Heyningen, V. (1998) Position effect in human genetic disease. Hum. Mol. Genet. 7, 1611–1618 23 Schweizer, J. et al. (1999) In vivo nuclease hypersensitivity studies reveal multiple sites of parental origin-dependent differential chromatin conformation in the 150 kb SNRPN transcription unit. Hum. Mol. Genet. 8, 555–566 24 Henchoz, S. et al. (1996) The dose of a putative ubiquitin-specific protease affects position-effect variegation in Drosophila melanogaster. Mol. Cell. Biol. 16, 5717–5725 25 Augusseau, S. et al. (1986) DiGeorge syndrome and 22q11 rearrangements. Hum. Genet. 74, 206 26 Carlson, C. et al. (1997) Molecular definition of 22q11 deletions in 151 velo-cardio-facial syndrome patients. Am. J. Hum. Genet. 61, 620–629 27 Levy, A. et al. (1995) Interstitial 22q11 microdeletion excluding the ADU breakpoint in a patient with DiGeorge syndrome. Hum. Mol. Genet. 4, 2417–2419 28 O’Donnell, H. et al. (1997) Detection of an atypical 22q11 deletion that has no overlap with the DiGeorge syndrome critical region. Am. J. Hum. Genet. 60, 1544–1548 29 Kurahashi, H. et al. (1996) Deletion mapping of 22q11 in CATCH22 syndrome: identification of a second critical region. Am. J. Hum. Genet. 58, 1377–1381

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A molecular pathway revealing a genetic basis for human cardiac and craniofacial defects.

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The combinatorial activities of Nkx2.5 and dHAND are essential for cardiac ventricle formation.

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The transcription factor dHAND is a downstream effector of BMPs in sympathetic neuron specification.

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عنوان ژورنال:
  • Trends in genetics : TIG

دوره 15 7  شماره 

صفحات  -

تاریخ انتشار 1999