Linked Life Data

9831130

Source:http://linkedlifedata.com/resource/pubmed/id/9831130

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pubmed-article:9831130pubmed:abstractTextThe nonclassical MHC class I HLA-G antigen is expressed in cytotrophoblasts during pregnancy and may play a role in inhibiting lysis by maternal natural killer cells. HLA-G gene transcription was analyzed in human fetal liver of 6-8 wk of gestation, a development stage where classical HLA class I expression is very reduced. We demonstrated that HLA-G transcription is undetectable in these cells and we investigated the molecular mechanisms that control the lack of HLA-G gene transcription. We compared protein interactions of nuclear extracts from first trimester fetal livers, YT2C2-PR (HLA-G negative) and JEG-3 (HLA-G positive) cell lines to a 244-bp EcoR I/Hind III DNA region located 1.2 kb from the HLA-G gene, previously shown to direct HLA-G expression in transgenic mouse placenta. A strong specific C7-factor was specifically detected in first trimester fetal liver that could account for the inhibition of HLA-G transcription. Interaction of C7-factor and cell-specific factors previously detected in YT2C2 cell line (C5, C6) with two distinct regulatory regions identify this 244-bp EcoR I/Hind III fragment as a putative target for inhibition of HLA-G transcription.lld:pubmed
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pubmed-article:9831130pubmed:dateRevised2011-11-17lld:pubmed
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pubmed-article:9831130pubmed:articleTitleSpecific binding of nuclear factors to the HLA-G gene promoter correlates with a lack of HLA-G transcripts in first trimester human fetal liver.lld:pubmed
pubmed-article:9831130pubmed:affiliationCEA, Service de Recherches en Hémato-immunologie, DSV, DRM, Centre Hayem, Hôpital Saint-Louis, Paris, France. moreau@dsvidf.cea.frlld:pubmed
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pubmed-article:9831130pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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