Evidence map›Paper›PMID 31586391›Full record

ArticleNucleic acids research2019

Chromatin Assembly Factor 1 (CAF-1) facilitates the establishment of facultative heterochromatin during pluripotency exit.

Liang Cheng, Xu Zhang, Yan Wang, Haiyun Gan, Xiaowei Xu, Xiangdong Lv, Xu Hua, Jianwen Que, Tamas Ordog, Zhiguo Zhang

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  6. Review
  7. Article
  8. Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026
    Review
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  13. Acute multi-level response to defectivebioRxiv : the preprint server for biology · 2024
    Article
  14. Article
  15. Article
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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

10 authors at 3 institutions in 1 country.

Liang ChengBiochemistry and Molecular Biology Track, Mayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, MN 55902, USA.
Xu ZhangInstitute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Yan WangBiochemistry and Molecular Biology Track, Mayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, MN 55902, USA.
Haiyun GanInstitute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Xiaowei XuInstitute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Xiangdong LvInstitute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Xu HuaInstitute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Jianwen QueDepartment of Medicine, Columbia University, New York, NY 10032, USA.
Tamas OrdogDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA.
Zhiguo ZhangInstitute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Cancer Genetics (United States) · USMayo Clinic · USColumbia University · US

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Parisa Tehranifar · 1985 to 2026
$115.3M
Physiological Characterization and Data Integration CoreP01DK068055 · NIDDK · MAYO CLINIC ROCHESTER · PI ORDOG, TAMAS · 2004 to 2019
$23.8M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
Mechanisms of Epigenetic inheritanceR35GM118015 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Zhiguo Zhang · 2016 to 2026
$9.5M
Interstitial Cells of Cajal in Diabetic GastropathyR01DK058185 · NIDDK · UNIVERSITY OF NEVADA RENO · PI ORDOG, TAMAS · 2002 to 2020
$5.2M
NCI NIH HHS P30 CA013696NIDDK NIH HHS P01 DK068055NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK058185NIGMS NIH HHS R35 GM118015
6 · The paper itself

Abstract

Establishment and subsequent maintenance of distinct chromatin domains during embryonic stem cell (ESC) differentiation are crucial for lineage specification and cell fate determination. Here we show that the histone chaperone Chromatin Assembly Factor 1 (CAF-1), which is recruited to DNA replication forks through its interaction with proliferating cell nuclear antigen (PCNA) for nucleosome assembly, participates in the establishment of H3K27me3-mediated silencing during differentiation. Deletion of CAF-1 p150 subunit impairs the silencing of many genes including Oct4, Sox2 and Nanog as well as the establishment of H3K27me3 at these gene promoters during ESC differentiation. Mutations of PCNA residues involved in recruiting CAF-1 to the chromatin also result in defects in differentiation in vitro and impair early embryonic development as p150 deletion. Together, these results reveal that the CAF-1-PCNA nucleosome assembly pathway plays an important role in the establishment of H3K27me3-mediated silencing during cell fate determination.

Indexed as

AnimalsCell DifferentiationCells, CulturedChromatin Assembly and DisassemblyChromatin Assembly Factor-1DNA ReplicationEmbryonic Stem CellsGene SilencingHeterochromatinHistone MethyltransferasesHistonesHumansMaleMiceMice, Inbred C57BLMice, Inbred NODChromatin Assembly Factor-1HeterochromatinHistone MethyltransferasesHistonesProliferating Cell Nuclear Antigen

Identifiers

PMID31586391
PMCPMC6868363
OpenAlexW2978748594

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.