Evidence map›Paper›PMID 21596989›Full record

ArticleScience (New York, N.Y.)2011

Chromatin "prepattern" and histone modifiers in a fate choice for liver and pancreas.

Cheng-Ran Xu, Philip A Cole, David J Meyers, Jay Kormish, Sharon Dent, Kenneth S Zaret

Open access · greenAbstract read
In one paragraph

Article in Science (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

112 citing papers in PubMed, 198 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. HumanPNAS nexus · 2024
    Article
  6. Review
  7. Editorial: Polycomb group (PcG) proteins in development and disease.Frontiers in cell and developmental biology · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. A single-cell-resolution fate map of endoderm reveals demarcation of pancreatic progenitors by cell cycle.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article

52 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 2 countries.

Cheng-Ran XuInstitute for Regenerative Medicine, Epigenetics Program, Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Philip A Cole
David J Meyers
Jay Kormish
Sharon Dent
Kenneth S Zaret
Johns Hopkins Medicine · USUniversity of Calgary · CA

Funding

Johns Hopkins Ion Channel CenterU54MH084691 · NIMH · JOHNS HOPKINS UNIVERSITY · PI LI, MIN · 2008 to 2012
$13.9M
Trans-acting Factors Causing Cell Specific Gene ControlR37GM036477 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI ZARET, KENNETH · 2006 to 2015
$5.4M
Mechanisms &Inhibition of Histone AcetyltransferasesR01GM062437 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COLE, PHILIP A · 2001 to 2012
$3.8M
Functions of Mammalian Histone ModifiersR01GM067718 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DENT, SHARON Y. R. · 2003 to 2018
$3.7M
Gene Regulatory Signals for Beta Cell DevelopmentU01DK072503 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI ZARET, KENNETH · 2005 to 2009
$3.5M
NIDDK NIH HHS U01 DK072503NIDDK NIH HHS U01DK072503NIGMS NIH HHS R01 GM062437NIGMS NIH HHS R01 GM067718NIGMS NIH HHS R37 GM036477NIGMS NIH HHS R37GM36477NIMH NIH HHS U54 MH084691NIMH NIH HHS U54MH084691
6 · The paper itself

Abstract

Transcriptionally silent genes can be marked by histone modifications and regulatory proteins that indicate the genes' potential to be activated. Such marks have been identified in pluripotent cells, but it is unknown how such marks occur in descendant, multipotent embryonic cells that have restricted cell fate choices. We isolated mouse embryonic endoderm cells and assessed histone modifications at regulatory elements of silent genes that are activated upon liver or pancreas fate choices. We found that the liver and pancreas elements have distinct chromatin patterns. Furthermore, the histone acetyltransferase P300, recruited via bone morphogenetic protein signaling, and the histone methyltransferase Ezh2 have modulatory roles in the fate choice. These studies reveal a functional "prepattern" of chromatin states within multipotent progenitors and potential targets to modulate cell fate induction.

Indexed as

Gene Expression Regulation, DevelopmentalAcetylationAnimalsBone Morphogenetic ProteinsCell Culture TechniquesCell DifferentiationCell SeparationChromatinChromatin ImmunoprecipitationEmbryonic DevelopmentEmbryonic InductionEndodermEnhancer of Zeste Homolog 2 ProteinHepatocytesHistone-Lysine N-MethyltransferaseHistonesBone Morphogenetic ProteinsChromatinEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseHistone-Lysine N-MethyltransferaseHistonesHomeodomain Proteinsp300-CBP-Associated Factorp300-CBP Transcription Factorspancreatic and duodenal homeobox 1 proteinPolycomb Repressive Complex 2Trans-ActivatorsTranscription Factors

Identifiers

PMID21596989
PMCPMC3128430
OpenAlexW2119076851

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.