Evidence map›Paper›PMID 25470594›Full record

ArticlePloS one2014

The epigenetic regulator CXXC finger protein 1 is essential for murine hematopoiesis.

Kristin T Chun, Binghui Li, Erika Dobrota, Courtney Tate, Jeong-Heon Lee, Shehnaz Khan, Laura Haneline, Harm HogenEsch, David G Skalnik

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The complex activities of the SET1/MLL complex core subunits in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. SET/MLL family proteins in hematopoiesis and leukemia.International journal of hematology · 2017
    Review
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Kristin T ChunHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America; Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America; Biology Department, Indiana University-Purdue University Indianapolis School of Science, Indianapolis, Indiana, United States of America.
Binghui LiHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Erika DobrotaHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Courtney TateHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America; Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Jeong-Heon LeeHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Shehnaz KhanHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Laura HanelineHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America; Departments of Microbiology & Immunology and Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Harm HogenEschDepartment of Comparative Pathobiology, Purdue University, West Lafayette, Indiana, United States of America.
David G SkalnikHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America; Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America; Biology Department, Indiana University-Purdue University Indianapolis School of Science, Indianapolis, Indiana, United States of America.
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicinePurdue University West Lafayette · US

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Jun Wan · 1999 to 2026
$59.3M
Immunology and Infectious Diseases Training ProgramT32AI060519 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARK H KAPLAN · 2004 to 2026
$6.0M
Role of Cul4A and ubiquitin in regulating hematopoiesisR01DK066603 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI CHUN, KRISTIN T · 2004 to 2008
$1.4M
NCI NIH HHS P30 CA082709NIAID NIH HHS T32 AI060519NIDDK NIH HHS R01 DK066603NIDDK NIH HHS R01 DK66603
6 · The paper itself

Abstract

CXXC finger protein 1 (Cfp1), encoded by the Cxxc1 gene, binds to DNA sequences containing an unmethylated CpG dinucleotide and is an epigenetic regulator of both cytosine and histone methylation. Cxxc1-null mouse embryos fail to gastrulate, and Cxxc1-null embryonic stem cells are viable but cannot differentiate, suggesting that Cfp1 is required for chromatin remodeling associated with stem cell differentiation and embryogenesis. Mice homozygous for a conditional Cxxc1 deletion allele and carrying the inducible Mx1-Cre transgene were generated to assess Cfp1 function in adult animals. Induction of Cre expression in adult animals led to Cfp1 depletion in hematopoietic cells, a failure of hematopoiesis with a nearly complete loss of lineage-committed progenitors and mature cells, elevated levels of apoptosis, and death within two weeks. A similar pathology resulted following transplantation of conditional Cxxc1 bone marrow cells into wild type recipients, demonstrating this phenotype is intrinsic to Cfp1 function within bone marrow cells. Remarkably, the Lin- Sca-1+ c-Kit+ population of cells in the bone marrow, which is enriched for hematopoietic stem cells and multi-potential progenitor cells, persists and expands in the absence of Cfp1 during this time frame. Thus, Cfp1 is necessary for hematopoietic stem and multi-potential progenitor cell function and for the developmental potential of differentiating hematopoietic cells.

Indexed as

Epigenesis, GeneticAnimalsAntigens, LyApoptosisBone Marrow CellsBone Marrow TransplantationCell DifferentiationCell LineageCell ProliferationCells, CulturedFemaleHematopoiesisHematopoietic Stem CellsImmunoblottingMaleMembrane ProteinsAntigens, LyCxxc1 protein, mouseLy6a protein, mouseMembrane ProteinsMx1 protein, mouseMyxovirus Resistance ProteinsProto-Oncogene Proteins c-kitTrans-Activators

Identifiers

PMID25470594
PMCPMC4254612
OpenAlexW2040890014

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.