ArticleMolecular and cellular biology2009
CXXC finger protein 1 contains redundant functional domains that support embryonic stem cell cytosine methylation, histone methylation, and differentiation.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 35 citations in OpenAlex.
- CFP1-mediated H3K4me3 broad domains control early B cell lineage fate determination.Nucleic acids research · 2026Article
- Physical and functional interaction between SET1/COMPASS complex component CFP-1 and a Sin3S HDAC complex in C. elegans.Nucleic acids research · 2019Article
- Epigenetic initiation of the TScience advances · 2019Article
- The SET1 Complex Selects Actively Transcribed Target Genes via Multivalent Interaction with CpG Island Chromatin.Cell reports · 2017Article
- PRDM9 interactions with other proteins provide a link between recombination hotspots and the chromosomal axis in meiosis.Molecular biology of the cell · 2017Article
- Computational inference of a genomic pluripotency signature in human and mouse stem cells.Biology direct · 2016Article
- CXXC finger protein 1 is critical for T-cell intrathymic development through regulating H3K4 trimethylation.Nature communications · 2016Article
- Transcript response of soft coral (Scleronephthya gracillimum) on exposure to polycyclic aromatic hydrocarbons.Environmental science and pollution research international · 2014Article
- MMDiff: quantitative testing for shape changes in ChIP-Seq data sets.BMC genomics · 2013Article
- Differentially expressed epigenome modifiers, including aurora kinases A and B, in immune cells in rheumatoid arthritis in humans and mouse models.Arthritis and rheumatism · 2013Article
- Cfp1 integrates both CpG content and gene activity for accurate H3K4me3 deposition in embryonic stem cells.Genes & development · 2012Article
- Selective targeting of histone methylation.Cell cycle (Georgetown, Tex.) · 2011Article
- The structural basis for selective binding of non-methylated CpG islands by the CFP1 CXXC domain.Nature communications · 2011Article
- The chromatin signaling pathway: diverse mechanisms of recruitment of histone-modifying enzymes and varied biological outcomes.Molecular cell · 2010Review
- GC-rich sequence elements recruit PRC2 in mammalian ES cells.PLoS genetics · 2010Article
- Coordinated chromatin control: structural and functional linkage of DNA and histone methylation.Biochemistry · 2010Review
- Experimental approaches to the study of epigenomic dysregulation in ageing.Experimental gerontology · 2010Review
- A conserved interaction between the SDI domain of Bre2 and the Dpy-30 domain of Sdc1 is required for histone methylation and gene expression.The Journal of biological chemistry · 2010Article
- CXXC finger protein 1 restricts the Setd1A histone H3K4 methyltransferase complex to euchromatin.The FEBS journal · 2010Article
- Article
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
CXXC finger protein 1 (Cfp1) is a regulator of both cytosine methylation and histone methylation. Murine embryonic stem (ES) cells lacking Cfp1 exhibit a decreased plating efficiency, decreased cytosine methylation, elevated global levels of histone H3-Lys4 trimethylation, and a failure to differentiate in vitro. Remarkably, transfection studies reveal that expression of either the amino half of Cfp1 (amino acids 1 to 367 [Cfp1(1-367)]) or the carboxyl half of Cfp1 (Cfp1(361-656)) is sufficient to correct all of the defects observed with ES cells that lack Cfp1. However, a point mutation (C169A) that abolishes DNA-binding activity of Cfp1 ablates the rescue activity of the Cfp1(1-367) fragment, and a point mutation (C375A) that abolishes the interaction of Cfp1 with the Setd1 histone H3-Lys4 methyltransferase complexes ablates the rescue activity of the Cfp1(361-656) fragment. Introduction of both the C169A and C375A point mutations ablates the rescue activity of the full-length Cfp1 protein. These results indicate that retention of either the Cfp1 DNA-binding domain or Setd1 interaction domain is required for Cfp1 rescue activity, and they illustrate the functional complexity of this critical epigenetic regulator. A model is presented for how epigenetic cross talk may explain the finding of redundant functional domains within Cfp1.
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.