ArticleMolecular and cellular biology2008
Bypassing the requirements for epigenetic modifications in gene transcription by increasing enhancer strength.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Role of nucleosome remodeling in neurodevelopmental and intellectual disability disorders.Frontiers in behavioral neuroscience · 2015Review
- Review
- Epigenetic memories: structural marks or active circuits?Cellular and molecular life sciences : CMLS · 2012Review
- Recruitment of histone deacetylase 3 to the interferon-A gene promoters attenuates interferon expression.PloS one · 2012Article
- Genomic analysis reveals a novel nuclear factor-κB (NF-κB)-binding site in Alu-repetitive elements.The Journal of biological chemistry · 2011Article
- Is an epigenetic switch the key to persistent extinction?Neurobiology of learning and memory · 2011Review
- Double null cells reveal that CBP and p300 are dispensable for p53 targets p21 and Mdm2 but variably required for target genes of other signaling pathways.Cell cycle (Georgetown, Tex.) · 2011Article
- CBP/p300 double null cells reveal effect of coactivator level and diversity on CREB transactivation.The EMBO journal · 2010Article
- Single cell analysis of transcriptional activation dynamics.PloS one · 2010Article
- Core promoter acetylation is not required for high transcription from the phosphoenolpyruvate carboxylase promoter in maize.Epigenetics & chromatin · 2009Article
- Hyperactivated NF-{kappa}B and AP-1 transcription factors promote highly accessible chromatin and constitutive transcription across the interleukin-6 gene promoter in metastatic breast cancer cells.Molecular and cellular biology · 2009Article
- Article
- Synergistic activation of HIV-1 expression by deacetylase inhibitors and prostratin: implications for treatment of latent infection.PloS one · 2009Article
- Global reorganization of replication domains during embryonic stem cell differentiation.PLoS biology · 2008Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our current concept postulates that histone acetylation is required for the recruitment of bromodomain-containing transcription complexes, such as the chromatin-remodeling machine SWI/SNF and the basal transcription factor TFIID. We generated simple NF-kappaB-dependent enhancers of increasing transcriptional strengths and found that the histone acetylation requirements for activation of transcription depended on the strengths of these enhancers. All enhancers function by recruiting SWI/SNF and TFIID to induce nucleosome sliding, a prerequisite for transcriptional activation. However, histone acetylation, although it occurs, is dispensable for TFIID and SWI/SNF recruitment by the strong enhancers, indicating that strong activators can overcome the chromatin barrier by directly recruiting the necessary transcriptional complexes. Weak enhancers depend on histone acetylation for recruitment, and this requirement is independent of a histone acetylation code. Thus, the need for nucleosome modifications is imposed on genes and translated according to the quality and strengths of the activators.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.