期刊
AMINO ACIDS
卷 38, 期 4, 页码 1067-1074出版社
SPRINGER WIEN
DOI: 10.1007/s00726-009-0315-y
关键词
Brain-derived neurotrophic factor; BDNF; Chromatin remodeling; Epigenetic modification; Histone; Methylation; HDAC; MeCP2
资金
- NIH [NIAAA Z01-AA00325]
- Defense Brain and Spinal Cord Injury Program [F-192EG-C1]
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [Z01AA000326] Funding Source: NIH RePORTER
Transcriptional regulation of the gene encoding brain-derived neurotrophic factor (BDNF) has been widely studied. However, an understanding of mechanisms modifying chromatin, events that are essential for controlling transcription, is rudimentary. We focused on two activation-dependent regions of the Bdnf gene physically linked to known transcription sites for exons 1 and 4. Using chromatin immunoprecipitation assays, we determined that N-methyl-d-aspartate (NMDA) receptor activation derepressed promoters 1 and 4-mediated transcription. This derepression correlated with reduced occupancy by histone deacetylase 1 and methyl cytosine-binding protein 2 of each promoter region near known transcription start sites in cultured hippocampal neurons. These changes did not occur at all sites upstream of transcription initiation. Taken together, these findings suggest that histone and other DNA-binding proteins are involved in remodeling of chromatin at some, but not all sites, within Bdnf promoters 1 and 4 and are associated with NMDA receptor-dependent increases in transcription.
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