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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2009-3-3
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pubmed:abstractText |
Disabled-2 (Dab2) is expressed in primitive endoderm cells as they are differentiating from the inner cell mass and dab2 deficiency in mice results in lethality at E5.5-E6.5 due to the disorganization of the endoderm layers. Here we show that Dab2 suppresses c-Fos expression in endoderm cells. A morphological normal primitive endoderm layer was observed in putative E5.5 dab2 (-/-):c-fos (-/-) embryos, indicating that the primitive endoderm defect due to the loss of Dab2 is rescued by deletion of the c-fos gene. The lethality of the double knockout embryos was delayed until E9.5-E10.5 and the defective embryos failed to undergo organogenesis. We conclude that Dab2 plays a role in epithelial organization by suppression of c-Fos expression and suggest that unsuppressed c-Fos can lead to disruption of primitive endoderm epithelial organization, yet an additional dab2 function is required for later organogenesis.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-10340382,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-10380922,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-10686601,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-10769163,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11039902,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11247302,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11359772,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11402055,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11577091,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11687976,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11906161,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11927540,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-11967127,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-12015763,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-12234931,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-12413896,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-12651740,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-12835387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-12893809,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-1423615,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-1473147,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-14981092,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-15280374,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-15960969,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-15960981,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-16308331,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-16540506,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-17339320,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-2502313,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-3141060,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-7545543,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-7775479,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-8039503,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-9009273,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-9338784,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-9338785,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19191218-9620555
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1058-8388
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pubmed:author |
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pubmed:copyrightInfo |
(c) 2009 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:volume |
238
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
514-23
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pubmed:dateRevised |
2011-9-26
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pubmed:meshHeading |
pubmed-meshheading:19191218-Adaptor Proteins, Vesicular Transport,
pubmed-meshheading:19191218-Animals,
pubmed-meshheading:19191218-Cell Differentiation,
pubmed-meshheading:19191218-Down-Regulation,
pubmed-meshheading:19191218-Embryo, Mammalian,
pubmed-meshheading:19191218-Embryonic Stem Cells,
pubmed-meshheading:19191218-Endoderm,
pubmed-meshheading:19191218-Gene Deletion,
pubmed-meshheading:19191218-Gene Expression Regulation, Developmental,
pubmed-meshheading:19191218-Genotype,
pubmed-meshheading:19191218-Mice,
pubmed-meshheading:19191218-Mice, Knockout,
pubmed-meshheading:19191218-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:19191218-Stem Cells
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pubmed:year |
2009
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pubmed:articleTitle |
C-Fos elimination compensates for disabled-2 requirement in mouse extraembryonic endoderm development.
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pubmed:affiliation |
Ovarian Cancer Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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