ArticleBMC genomics2015
CGGBP1 mitigates cytosine methylation at repetitive DNA sequences.
Article in BMC genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- CGGBP1-Regulated Heterogeneous C-T Transition Rates Correlate with G-quadruplex Potential of Terrestrial Vertebrate Genomes.Journal of molecular evolution · 2026Article
- The amniote-conserved DNA-binding domain of CGGBP1 restricts cytosine methylation of transcription factor binding sites in proximal promoters to regulate gene expression.BMC genomic data · 2024Article
- G-quadruplex landscape and its regulation revealed by a new antibody capture method.Oncotarget · 2024Article
- Chimeric chromosome landscapes of human somatic cell cultures show dependence on stress and regulation of genomic repeats by CGGBP1.Oncotarget · 2022Article
- CGGBP1-regulated cytosine methylation at CTCF-binding motifs resists stochasticity.BMC genetics · 2020Article
- CGGBP1 regulates CTCF occupancy at repeats.Epigenetics & chromatin · 2019Article
- Dynamic bimodal changes in CpG and non-CpG methylation genome-wide upon CGGBP1 loss-of-function.BMC research notes · 2018Article
- Dysregulation of DNA methylation induced by past arsenic treatment causes persistent genomic instability in mammalian cells.Environmental and molecular mutagenesis · 2016Article
- CGGBP1--an indispensable protein with ubiquitous cytoprotective functions.Upsala journal of medical sciences · 2015Review
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Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCGGBP1 is a repetitive DNA-binding transcription regulator with target sites at CpG-rich sequences such as CGG repeats and Alu-SINEs and L1-LINEs. The role of CGGBP1 as a possible mediator of CpG methylation however remains unknown. At CpG-rich sequences cytosine methylation is a major mechanism of transcriptional repression. Concordantly, gene-rich regions typically carry lower levels of CpG methylation than the repetitive elements. It is well known that at interspersed repeats Alu-SINEs and L1-LINEs high levels of CpG methylation constitute a transcriptional silencing and retrotransposon inactivating mechanism.
resultsHere, we have studied genome-wide CpG methylation with or without CGGBP1-depletion. By high throughput sequencing of bisulfite-treated genomic DNA we have identified CGGBP1 to be a negative regulator of CpG methylation at repetitive DNA sequences. In addition, we have studied CpG methylation alterations on Alu and L1 retrotransposons in CGGBP1-depleted cells using a novel bisulfite-treatment and high throughput sequencing approach.
conclusionsThe results clearly show that CGGBP1 is a possible bidirectional regulator of CpG methylation at Alus, and acts as a repressor of methylation at L1 retrotransposons.
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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.