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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2008-4-30
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pubmed:abstractText |
Many genes are known to function in a region-specific manner in the developing secondary palate. We have previously shown that Shox2-deficient embryos die at mid-gestation stage and develop an anterior clefting phenotype. Here, we show that mice carrying a conditional inactivation of Shox2 in the palatal mesenchyme survive the embryonic and neonatal lethality, but develop a wasting syndrome. Phenotypic analyses indicate a delayed closure of the secondary palate at the anterior end, leading to a failed fusion of the primary and secondary palates. Consistent with a role proposed for Shox2 in skeletogenesis, Shox2 inactivation causes a significantly reduced bone formation in the hard palate, probably due to a down-regulation of Runx2 and Osterix. We conclude that the secondary palatal shelves are capable of fusion with each other, but fail to fuse with the primary palate in a developmentally delayed manner. Mice carrying an anterior cleft can survive neonatal lethality.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Fgf10 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Fibroblast Growth Factor 10,
http://linkedlifedata.com/resource/pubmed/chemical/High Mobility Group Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/SOX9 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/SOX9 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Shox2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Sox9 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1058-8388
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
237
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1509-16
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pubmed:dateRevised |
2011-6-8
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pubmed:meshHeading |
pubmed-meshheading:18393307-Animals,
pubmed-meshheading:18393307-Cleft Palate,
pubmed-meshheading:18393307-Fibroblast Growth Factor 10,
pubmed-meshheading:18393307-High Mobility Group Proteins,
pubmed-meshheading:18393307-Homeodomain Proteins,
pubmed-meshheading:18393307-Humans,
pubmed-meshheading:18393307-In Situ Hybridization,
pubmed-meshheading:18393307-Mesoderm,
pubmed-meshheading:18393307-Mice,
pubmed-meshheading:18393307-Mice, Knockout,
pubmed-meshheading:18393307-Mice, Transgenic,
pubmed-meshheading:18393307-Osteogenesis,
pubmed-meshheading:18393307-Palate,
pubmed-meshheading:18393307-Phenotype,
pubmed-meshheading:18393307-SOX9 Transcription Factor,
pubmed-meshheading:18393307-Survival Rate,
pubmed-meshheading:18393307-Tissue Culture Techniques,
pubmed-meshheading:18393307-Transcription Factors
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pubmed:year |
2008
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pubmed:articleTitle |
Mice with an anterior cleft of the palate survive neonatal lethality.
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pubmed:affiliation |
Section of Oral Biology, The Ohio State University College of Dentistry, Columbus, Ohio 43210, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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