Abstract
Oestrogen receptor-alpha (ERalpha)-regulated transcription in breast cancer cells involves protein co-factors that contribute to the regulation of chromatin structure. These include co-factors with the potential to regulate histone modifications such as acetylation or methylation, and therefore the transcriptional state of target genes. Although much of the information regarding the interaction of specific co-factors with ER has been generated by studying specific promoter regions, we now have an improved understanding of the nature of these interactions and are better placed to relate these with ER activity and potentially with the activity of breast cancer drugs, including tamoxifen.
MeSH terms
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Amino Acid Sequence
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Carrier Proteins / pharmacology
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Chromatin / metabolism*
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Chromatin Immunoprecipitation
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Corticosterone
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Estrogen Receptor alpha / chemistry
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Estrogen Receptor alpha / physiology*
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Humans
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Models, Biological
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Nuclear Proteins / pharmacology
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Nuclear Receptor Co-Repressor 1
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Repressor Proteins / pharmacology
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Tamoxifen / pharmacology
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Transcription, Genetic*
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Transcriptional Activation
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Trefoil Factor-1
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Tumor Suppressor Proteins / pharmacology
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p300-CBP Transcription Factors / pharmacology
Substances
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Carrier Proteins
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Chromatin
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Estrogen Receptor alpha
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NCOR1 protein, human
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Nuclear Proteins
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Nuclear Receptor Co-Repressor 1
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Repressor Proteins
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TFF1 protein, human
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Trefoil Factor-1
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Tumor Suppressor Proteins
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Tamoxifen
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p300-CBP Transcription Factors
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Corticosterone