ArticleMolecular and cellular biology2006
Differential recruitment of methylated CpG binding domains by the orphan receptor GCNF initiates the repression and silencing of Oct4 expression.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- Regulation of Oct4 in stem cells and neural crest cells.Birth defects research · 2022Review
- DNA methylation in promoter regions of genes involved in the reproductive and metabolic function of children born to women with PCOS.Epigenetics · 2020Article
- Acetylation- and Methylation-Related Epigenetic Proteins in the Context of Their Targets.Genes · 2017Review
- MiR-134-Mbd3 axis regulates the induction of pluripotency.Journal of cellular and molecular medicine · 2016Article
- Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells.Journal of cellular physiology · 2013Article
- Analysis method of epigenetic DNA methylation to dynamically investigate the functional activity of transcription factors in gene expression.BMC genomics · 2012Article
- Differential expression of Oct4 in HPV-positive and HPV-negative cervical cancer cells is not regulated by DNA methyltransferase 3A.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011Article
- Nuclear reprogramming in mouse primordial germ cells: epigenetic contribution.Stem cells international · 2011Article
- Targeting of de novo DNA methylation throughout the Oct-4 gene regulatory region in differentiating embryonic stem cells.PloS one · 2010Article
- Donor-host mitochondrial compatibility improves efficiency of bovine somatic cell nuclear transfer.BMC developmental biology · 2010Article
- Minireview: Nuclear receptors, hematopoiesis, and stem cells.Molecular endocrinology (Baltimore, Md.) · 2010Review
- The N-terminus of histone H3 is required for de novo DNA methylation in chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Article
- DNA methylation and methyl-CpG binding proteins: developmental requirements and function.Chromosoma · 2009Review
- Cdk2ap1 is required for epigenetic silencing of Oct4 during murine embryonic stem cell differentiation.The Journal of biological chemistry · 2009Article
- Suppression of Oct4 by germ cell nuclear factor restricts pluripotency and promotes neural stem cell development in the early neural lineage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Tissue specific differentially methylated regions (TDMR): Changes in DNA methylation during development.Genomics · 2009Article
- Cloning and Characterization of 3.1kb Promoter Region of the Oct4 Gene from the Fischer 344 Rat.The open stem cell journal · 2009Article
- Article
- DNA methylation in development and human disease.Mutation research · 2008Review
Corrections and comments
- Retraction · 2009-04-01Concerns/Issues about Image · Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by ORI · Investigation by Third Party · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · · For details about the investigation findings, please see: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019639/ .;
- Commented on by
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The pluripotent factor Oct4 is a key transcription factor that maintains embryonic stem (ES) cell self-renewal and is down-regulated upon the differentiation of ES cells and silenced in somatic cells. A combination of cis elements, transcription factors, and epigenetic modifications, such as DNA methylation, are involved in the regulation of Oct4 gene expression. Here we show that the orphan nuclear receptor GCNF initiates Oct4 repression and DNA methylation by the differential recruitment of MBD (methylated CpG binding domain) factors to the promoter. Compared with wild-type ES cells and gastrulating embryos, Oct4 repression is lost and its proximal promoter is significantly hypomethylated in RA-differentiated GCNF(-/-) ES cells. The Oct4 gene is reexpressed in some somatic cells of GCNF(-/-) embryos, showing that it has not been properly silenced coincident with reduced DNA methylation of its promoter. Efforts to characterize mediators of GCNF's repressive function and DNA methylation of the Oct4 promoter identified methyl-DNA binding proteins, MBD3 and MBD2, as GCNF-interacting factors. In P19 and ES cells, upon differentiation, endogenous GCNF binds to the Oct4 proximal promoter and differentially recruits MBD3 and MBD2. In differentiated GCNF(-/-) ES cells, recruitment of MBD3 and MBD2 to the Oct4 promoter is lost, and repression of Oct4 expression and DNA methylation fails to occur. RNA interference-mediated knockdown of MBD3 and/or MBD2 expression results in reduced Oct4 repression in differentiated P19 and ES cells. Repression of Oct4 expression and recruitment of MBD3 are maintained in de novo DNA methylation-deficient ES cells (Dnmt3A/3B-null cells), while MBD2 recruitment is lost. Thus, recruitment of MBD3 and MBD2 by GCNF links two events, gene-specific repression and DNA methylation, which occur differentially at the Oct4 promoter. GCNF initiates the repression and epigenetic modification of Oct4 gene during ES cell differentiation.
Indexed as
Identifiers
What OpenQuestion holds
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.