CpG methylation inhibits proenkephalin gene expression and binding of the transcription factor AP-2.
AUTOR(ES)
Comb, M
RESUMO
DNA methylation at HpaII (CmCGG) sites inhibits expression of a human proenkephalin-CAT fusion gene when it is transiently expressed in CV-1 cells or stably expressed in C6-glioma cells. The inhibitory effects of HpaII methylation have been mapped to a site within the human proenkephalin promoter located at position -72 relative to the start site of transcription. This region spans a cAMP and phorbol ester inducible enhancer and methylation at this position inhibits both basal transcription and transcription induced by either cAMP or TPA. The HpaII site is located within an element which binds the transcription factor AP-2. In vitro methylation at this HpaII site inhibits the binding of AP-2. These results suggest that CpG methylation inhibits proenkephalin gene expression by directly interfering with the binding of a positively acting transcription factor previously shown to be essential for maximal basal, cAMP, and TPA inducible transcription.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=331101Documentos Relacionados
- Roles of Cell Division and Gene Transcription in the Methylation of CpG Islands
- Assessment of clusters of transcription factor binding sites in relationship to human promoter, CpG islands and gene expression
- CpG methylation directly inhibits binding of the human papillomavirus type 16 E2 protein to specific DNA sequences.
- Regulation of Pdha-2 expression is mediated by proximal promoter sequences and CpG methylation.
- Predicting aberrant CpG island methylation