ArticleMolecular and cellular biology2011
Distinct roles of DMAP1 in mouse development.
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 22 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
22 citing papers in PubMed, 41 citations in OpenAlex.
- Biallelic inactivating variants in the chromatin remodeler DMAP1 cause a syndromic neurodevelopmental disorder.The Journal of clinical investigation · 2026Article
- Chromatin remodeling activity of EP400 safeguards chromosomal stability by preventing CENP-A mislocalization.Cell reports · 2025Article
- Review
- Noncanonical action of circadian clock genes controls winter diapause entry via the NuA4/TIP60 complex inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- The DNA methyltransferase DMAP1 is required for tissue maintenance and planarian regeneration.Developmental biology · 2024Article
- The DNA Methyltransferase DMAP1 is Required for Tissue Maintenance and Planarian Regeneration.bioRxiv : the preprint server for biology · 2024Article
- Article
- CRISPR-Knockout Screen Identifies Dmap1 as a Regulator of Chemically Induced Reprogramming and Differentiation of Cardiac Progenitors.Stem cells (Dayton, Ohio) · 2019Article
- Article
- Impact of Maternal Age on Oocyte and Embryo Competence.Frontiers in endocrinology · 2018Review
- KATapulting toward Pluripotency and Cancer.Journal of molecular biology · 2017Review
- Lysine Acetylation and Deacetylation in Brain Development and Neuropathies.Genomics, proteomics & bioinformatics · 2017Review
- Allosteric control of mammalian DNA methyltransferases - a new regulatory paradigm.Nucleic acids research · 2016Review
- The Role of Maternal-Effect Genes in Mammalian Development: Are Mammalian Embryos Really an Exception?Stem cell reviews and reports · 2016Review
- A draft map of the mouse pluripotent stem cell spatial proteome.Nature communications · 2016Article
- Stem Cell Models to Investigate the Role of DNA Methylation Machinery in Development of Neuropsychiatric Disorders.Stem cells international · 2016Review
- The DNMT1 intrinsically disordered domain regulates genomic methylation during development.Genetics · 2015Article
- The chromatin regulator DMAP1 modulates activity of the nuclear factor B (NF-B) transcription factor Relish in the Drosophila innate immune response.The Journal of biological chemistry · 2014Article
- Totipotency: what it is and what it is not.Stem cells and development · 2014Article
- Chromatin-remodeling complex specificity and embryonic vascular development.Cellular and molecular life sciences : CMLS · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
DMAP1 (DNMT1-associated protein 1) is a member of the TIP60-p400 complex that maintains embryonic stem (ES) cell pluripotency and a complex containing the somatic form of DNA methyltransferase 1 (DNMT1s). DMAP1 interacts with DNMT1s through a domain that is absent in Dnmt1(V)(/)(V) mice expressing just the oocyte form (DNMT1o). A Dmap1-null allele was generated to study the role of DMAP1 in development. Consistent with the phenotypes of loss of other members of the TIP60-p400 complex, Dmap1(-/-) mice died during preimplantation in both Dnmt1(+/+) and Dnmt1(V)(/)(V) backgrounds. Unexpectedly, in the Dnmt1(V)(/)(V) background, Dmap1(+/-) parents produced mainly Dmap1(+/-) mice. Most Dmap1(+/+) progeny died during midgestation, with loss of DNA methylation on imprinted genes, suggesting that DMAP1 influences maintenance methylation mediated by DNMT1o. In this regard, a DMAP1-DNMT1o complex was detected in ES cells when DNMT1o was stably expressed but not when transiently expressed, indicating a novel interaction between DMAP1 and DNMT1o. These results suggest that DMAP1-DNMT1s and DMAP1-DNMT1o interactions are essential for normal development and that DMAP1-DNMT1o complexes are not readily formed in the embryo. Therefore, DMAP1 mediates distinct preimplantation epigenetic reprogramming processes: TIP60-p400 nucleosome remodeling and DNMT1 maintenance methylation.
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.