Evidence map›Paper›PMID 28692904›Full record

ReviewCurrent opinion in genetics & development2017

Emerging roles of the histone chaperone CAF-1 in cellular plasticity.

Sihem Cheloufi, Konrad Hochedlinger

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in genetics & development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Histone Chaperones as Cardinal Players in Development.Frontiers in cell and developmental biology · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cell Fate Decisions in the Wake of Histone H3 Deposition.Frontiers in cell and developmental biology · 2021
    Review
  17. Induced Neurons From Germ Cells inFrontiers in neuroscience · 2021
    Review
  18. Review
  19. Review
  20. 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

2 authors at 2 institutions in 1 country.

Sihem CheloufiDepartment of Molecular Biology, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA; Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA; Cancer Center, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, 1350 Massachusetts Avenue, Cambridge, MA 02138, USA.
Konrad HochedlingerDepartment of Molecular Biology, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA; Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA; Cancer Center, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, 1350 Massachusetts Avenue, Cambridge, MA 02138, USA. Electronic address: khochedlinger@mgh.harvard.edu.
Harvard Stem Cell Institute · USMassachusetts General Hospital · US

Funding

Transcription Factor Induced ReprogrammingR01HD058013 · NICHD · MASSACHUSETTS GENERAL HOSPITAL · PI HOCHEDLINGER, KONRAD · 2010 to 2019
$4.4M
NICHD NIH HHS R01 HD058013
6 · The paper itself

Abstract

During embryonic development, cells become progressively restricted in their differentiation potential. This is thought to be regulated by dynamic changes in chromatin structure and associated modifications, which act together to stabilize distinct specialized cell lineages. Remarkably, differentiated cells can be experimentally reprogrammed to a stem cell-like state or to alternative lineages. Thus, cellular reprogramming provides a valuable platform to study the mechanisms that normally safeguard cell identity and uncover factors whose manipulation facilitates cell fate transitions. Recent work has identified the chromatin assembly factor complex CAF-1 as a potent barrier to cellular reprogramming. In addition, CAF-1 has been implicated in the reversion of pluripotent cells to a totipotent-like state and in various lineage conversion paradigms, suggesting that modulation of CAF-1 levels may endow cells with a developmentally more plastic state. Here, we review these exciting results, discuss potential mechanisms and speculate on the possibility of exploiting chromatin assembly pathways to manipulate cell identity.

Indexed as

AnimalsCell DifferentiationCell LineageCell PlasticityCellular ReprogrammingChromatinChromatin Assembly and DisassemblyEmbryonic DevelopmentGene Expression Regulation, DevelopmentalHumansTranscription FactorsChromatinCNOT8 protein, humanTranscription Factors

Identifiers

PMID28692904
PMCPMC5813839
OpenAlexW2724942720

What OpenQuestion holds

Textmetadata
LicenceTDM
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.