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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1993-6-1
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pubmed:abstractText |
Polymorphic as well as HLA-F and -G genes are repressed in the human cell line JAR, derived from a tumor of trophoblast origin. By contrast, the HLA-E gene as well as the non-HLA novel coding-sequence, R1, located 5' to HLA-E, both remain transcriptionally active. We first demonstrated the role of DNA methylation in the repression of class I genes (except HLA-E) in JAR by the use of the 5-Azacytidine demethylating agent. Following treatment, JAR clones reexpressed polymorphic class I transcripts and cell surface alpha chains. Using methylation-sensitive rare cutter enzymes on JAR genomic DNA, followed by classical or pulse field gel electrophoresis and hybridization with HLA locus-specific probes, we found methylated CpG islands in the 5' region of all class I genes, except for HLA-E. These results, establishing an inverse relationship between states of methylation and transcriptional activity within the MHC class I chromosomal region in JAR, and the observations that the HLA-E and R1 genes were ubiquitously expressed, suggest that the HLA-E chromosomal domain might have functional importance including the presence of housekeeping genes.
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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/Azacitidine,
http://linkedlifedata.com/resource/pubmed/chemical/HLA Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-E antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Oligodeoxyribonucleotides,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:issn |
0093-7711
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:geneSymbol |
HLA-E
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
117-30
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7683306-Azacitidine,
pubmed-meshheading:7683306-Base Sequence,
pubmed-meshheading:7683306-Choriocarcinoma,
pubmed-meshheading:7683306-Electrophoresis, Gel, Pulsed-Field,
pubmed-meshheading:7683306-Gene Expression Regulation,
pubmed-meshheading:7683306-Genes,
pubmed-meshheading:7683306-Genes, MHC Class I,
pubmed-meshheading:7683306-HLA Antigens,
pubmed-meshheading:7683306-Histocompatibility Antigens Class I,
pubmed-meshheading:7683306-Methylation,
pubmed-meshheading:7683306-Molecular Sequence Data,
pubmed-meshheading:7683306-Oligodeoxyribonucleotides,
pubmed-meshheading:7683306-Polymorphism, Genetic,
pubmed-meshheading:7683306-Polymorphism, Restriction Fragment Length,
pubmed-meshheading:7683306-RNA, Messenger,
pubmed-meshheading:7683306-Restriction Mapping,
pubmed-meshheading:7683306-Transcription, Genetic,
pubmed-meshheading:7683306-Tumor Cells, Cultured
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pubmed:year |
1993
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pubmed:articleTitle |
HLA-E is the only class I gene that escapes CpG methylation and is transcriptionally active in the trophoblast-derived human cell line JAR.
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pubmed:affiliation |
Laboratoire d'Immunologie, Faculté de Médecine de la Timone, Marseille, France.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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