Circadian abnormalities in mouse models of smith-magenis syndrome: Evidence for involvement ofRAI1
Author:
Affiliation:
1. Department of Molecular and Human Genetics; Baylor College of Medicine; Houston, Texas
Publisher
Wiley
Subject
Genetics(clinical),Genetics
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1002/ajmg.a.35941/fullpdf
Reference38 articles.
1. Appearances can be deceiving: Phenotypes of knockout mice;Barbaric;Brief Funct Genomic Proteomic,2007
2. Mutations of RAI1, a PHD-containing protein, in nondeletion patients with Smith-Magenis syndrome;Bi;Hum Genet,2004
3. Inactivation of Rai1 in mice recapitulates phenotypes observed in chromosome engineered mouse models for Smith-Magenis syndrome;Bi;Hum Mol Genet,2005
4. RAI1 point mutations, CAG repeat variation, and SNP analysis in non-deletion Smith-Magenis syndrome;Bi;Am J Med Genet Part A,2006
5. Rai1 deficiency in mice causes learning impairment and motor dysfunction, whereas Rai1 heterozygous mice display minimal behavioral phenotypes;Bi;Hum Mol Genet,2007
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