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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
37
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pubmed:dateCreated |
1994-10-11
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pubmed:abstractText |
Retinoic acid (RA), we show, induces in peripheral blood mononuclear cells a transient wave of newly transcribed, unstable interleukin-1 alpha (IL-1 alpha) and IL-1 beta mRNA. Tumor necrosis factor-alpha mRNA, by contrast, is expressed in multiple waves. IL-1 genes are primary targets for RA. Most IL-1 beta gene transcription induced by RA fails to yield mature mRNA. Instead, precursor transcripts accumulate, detected by ribonuclease protection analysis. The flow of precursors into IL-1 beta mRNA becomes inhibited during induction. When translation is blocked, e.g. by cycloheximide, expression of IL-1 beta mRNA is superinduced by 2 orders of magnitude. Superinduction is dependent on transcription, yet is unaccompanied by increased primary transcription or mRNA stability. Instead, processing of unstable IL-1 beta precursor transcripts into mature mRNA is greatly facilitated. Control is not narrowly localized within precursors: splicing of distinct exons and intron excision are enhanced by cycloheximide. Pre-mRNA processing thus is a limiting step in RA-induced IL-1 beta gene expression. This regulation is specific for RA: when induced by phorbol ester, IL-1 beta gene expression is also superinduced by cycloheximide but that response is accompanied by enhanced mRNA stability. Thus, IL-1 beta gene transcription is induced by RA, yet, unlike for other primary target genes, mRNA expression is regulated at pre-mRNA processing.
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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/Cycloheximide,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/RNA Precursors,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
16
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pubmed:volume |
269
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pubmed:geneSymbol |
IL-1&agr;,
IL-1&bgr;,
TNF-&agr;
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
23141-9
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:8083217-Cells, Cultured,
pubmed-meshheading:8083217-Cycloheximide,
pubmed-meshheading:8083217-Gene Expression Regulation,
pubmed-meshheading:8083217-Humans,
pubmed-meshheading:8083217-Interleukin-1,
pubmed-meshheading:8083217-RNA, Messenger,
pubmed-meshheading:8083217-RNA Precursors,
pubmed-meshheading:8083217-RNA Processing, Post-Transcriptional,
pubmed-meshheading:8083217-Tetradecanoylphorbol Acetate,
pubmed-meshheading:8083217-Transcription, Genetic,
pubmed-meshheading:8083217-Tretinoin,
pubmed-meshheading:8083217-Tumor Necrosis Factor-alpha
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pubmed:year |
1994
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pubmed:articleTitle |
Induction of human interleukin-1 gene expression by retinoic acid and its regulation at processing of precursor transcripts.
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pubmed:affiliation |
Department of Molecular Virology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
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pubmed:publicationType |
Journal Article
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