Source:http://linkedlifedata.com/resource/pubmed/id/11741941
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2002-2-18
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pubmed:abstractText |
The transcription factor AP-2 alpha has been implicated as a cell type-specific regulator of gene expression during vertebrate embryogenesis based on its expression pattern in neural crest cells, ectoderm, and the nervous system in mouse and frog embryos. AP-2 alpha is prominently expressed in cranial neural crest cells, a population of cells that migrate from the lateral margins of the brain plate during closure of the neural tube at day 8-9 of embryonic development. Homozygous AP-2 alpha mutant mice die perinatally with cranio-abdominoschisis, full facial clefting, and defects in cranial ganglia and sensory organs, indicating the importance of this gene for proper development. By using a subtractive cloning approach, we identified a set of genes repressed by AP-2 alpha that are described to retard cellular proliferation and induce differentiation and apoptosis. We show that these target genes are prematurely expressed in AP-2 alpha mutant mice. One of the genes isolated, the Krüppel-box transcription factor KLF-4 implicated in induction of terminal differentiation and growth regulation, is found expressed in mutant embryonic fibroblasts. We show that fibroblasts lacking AP-2 alpha display retarded growth but no enhanced apoptosis. Based on these data we suggest that AP-2 alpha might be required for cell proliferation by suppression of genes inducing terminal differentiation, apoptosis, and growth retardation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tcfap2a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-2,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
22
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pubmed:volume |
277
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6637-44
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11741941-Animals,
pubmed-meshheading:11741941-Cell Differentiation,
pubmed-meshheading:11741941-Cell Division,
pubmed-meshheading:11741941-Cloning, Molecular,
pubmed-meshheading:11741941-DNA, Complementary,
pubmed-meshheading:11741941-DNA-Binding Proteins,
pubmed-meshheading:11741941-Fibroblasts,
pubmed-meshheading:11741941-Gene Expression Regulation, Developmental,
pubmed-meshheading:11741941-Gene Library,
pubmed-meshheading:11741941-Mice,
pubmed-meshheading:11741941-Nervous System,
pubmed-meshheading:11741941-Polymerase Chain Reaction,
pubmed-meshheading:11741941-Proteins,
pubmed-meshheading:11741941-Ranidae,
pubmed-meshheading:11741941-Repressor Proteins,
pubmed-meshheading:11741941-Transcription, Genetic,
pubmed-meshheading:11741941-Transcription Factor AP-2,
pubmed-meshheading:11741941-Transcription Factors
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pubmed:year |
2002
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pubmed:articleTitle |
A subtractive gene expression screen suggests a role of transcription factor AP-2 alpha in control of proliferation and differentiation.
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pubmed:affiliation |
Forschungszentrum Karlsruhe, ITG, Hermann von Helmholtz Platz 1, 76344 Eggenstein-Leopoldshafen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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