ArticleMolecular and cellular biology2011
Prevention of transcriptional silencing by a replicator-binding complex consisting of SWI/SNF, MeCP1, and hnRNP C1/C2.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- Replication timing and nuclear structure.Current opinion in cell biology · 2018Review
- Phosphorylated SIRT1 associates with replication origins to prevent excess replication initiation and preserve genomic stability.Nucleic acids research · 2017Article
- Order from clutter: selective interactions at mammalian replication origins.Nature reviews. Genetics · 2017Review
- Regulation of Replication Origins.Advances in experimental medicine and biology · 2017Review
- A replicator-specific binding protein essential for site-specific initiation of DNA replication in mammalian cells.Nature communications · 2016Article
- Replication origins: determinants or consequences of nuclear organization?Current opinion in genetics & development · 2016Review
- Distinct epigenetic features of differentiation-regulated replication origins.Epigenetics & chromatin · 2016Article
- The DNA repair endonuclease Mus81 facilitates fast DNA replication in the absence of exogenous damage.Nature communications · 2015Article
- Chromatin structure and replication origins: determinants of chromosome replication and nuclear organization.Journal of molecular biology · 2014Review
- Article
- Methylation of histone H3 on lysine 79 associates with a group of replication origins and helps limit DNA replication once per cell cycle.PLoS genetics · 2013Article
- Article
- The regulation of AβPP expression by RNA-binding proteins.Ageing research reviews · 2012Review
- The chromatin backdrop of DNA replication: lessons from genetics and genome-scale analyses.Biochimica et biophysica acta · 2012Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Transcriptional silencing selectively impedes gene expression. Silencing is often accompanied by replication delay and can be prevented by replicator sequences. Here we report a replicator-binding protein complex involved in the prevention of transcriptional silencing. The protein complex interacts with an essential asymmetric region within the human β-globin Rep-P replicator and includes hnRNP C1/C2, SWI/SNF complex, and MeCP1, which are members of the locus control region (LCR)-associated remodeling complex (LARC). Interaction between LARC and Rep-P prevented transcriptional silencing and replication delay. Transgenes that did not contain the asymmetric LARC-binding region of Rep-P replicated late and exhibited stable silencing that could not be affected by a DNA methylation inhibitor. In contrast, transgenes that contain a mutation of the asymmetric region of Rep-P that could not bind LARC exhibited a silent state that could transiently be reactivated by DNA demethylation. The effect of DNA demethylation was transient, and prolonged exposure to a methylation inhibitor induced distinct, stable, methylation-independent silencing. These observations suggest that the interaction of LARC complex with replicators plays a role in preventing gene silencing and provides support for a novel, epigenetic mechanism of resistance to methylation inhibitors.
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Registered trials
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.