Abstract
The expression of the endogenous CRF gene was examined in the human neuroblastoma cell line, BE(2)-M17. In this cell line, treatment with retinoic acid induces CRF mRNA transcription. We examined the requirement for the POU transcription factor, Bm-2, for this response. We confirmed that Bm-2 is expressed in retinoic acid-induced BE(2)-M17 cells. Expression of antisense Bm-2 message aborted the retinoic acid-mediated induction of CRF transcription. However, overexpression of Bm-2 was not sufficient for CRF expression in the absence of retinoic acid. These experiments support the hypothesis that Bm-2 is an intermediary for retinoic acid-induced CRF expression.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Binding Sites
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Blotting, Southern
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Corticotropin-Releasing Hormone / genetics*
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DNA / metabolism
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Gene Expression* / drug effects
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Genes, Reporter
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HeLa Cells
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Homeodomain Proteins
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Humans
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Mutagenesis, Site-Directed
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Neuroblastoma
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Neurons / metabolism*
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POU Domain Factors
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Promoter Regions, Genetic
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RNA, Antisense / genetics
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RNA, Messenger / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Transcription Factors / genetics
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Transcription Factors / physiology*
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Transfection
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Tretinoin / pharmacology
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Tumor Cells, Cultured
Substances
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Homeodomain Proteins
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POU Domain Factors
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RNA, Antisense
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RNA, Messenger
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Transcription Factors
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transcription factor Brn-2
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Tretinoin
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DNA
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Corticotropin-Releasing Hormone