Evidence map›Paper›PMID 21402699›Full record

ArticleThe Journal of biological chemistry2011

Endothelial Jarid2/Jumonji is required for normal cardiac development and proper Notch1 expression.

Matthew R Mysliwiec, Emery H Bresnick, Youngsook Lee

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

48 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Epigenetics.Advances in experimental medicine and biology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Embryonic Expression of NrasFrontiers in cell and developmental biology · 2021
    Article
  16. Review
  17. Endothelial-Myocardial Angiocrine Signaling in Heart Development.Frontiers in cell and developmental biology · 2021
    Review
  18. Tumor mutation burden andAnnals of translational medicine · 2020
    Article
  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

3 authors at 1 institution in 1 country.

Matthew R MysliwiecDepartment of Anatomy, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.
Emery H Bresnick
Youngsook Lee
University of Wisconsin–Madison · US

Funding

Hematopoietic Regulation via GATA SwitchesR01DK068634 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI Emery H. Bresnick · 2006 to 2026
$7.5M
Roles of transcription factors in cardiac developmentR01HL067050 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI LEE, YOUNGSOOK · 2002 to 2009
$2.7M
Hematopoietic Regulation Via GATA SwitchesR56DK068634 · NIDDK · UNIVERSITY OF WISCONSIN MADISON · PI BRESNICK, EMERY H. · 2005 to 2005
$109k
NHLBI NIH HHS HL67050NHLBI NIH HHS R01 HL067050NIDDK NIH HHS DK068634NIDDK NIH HHS R01 DK068634NIDDK NIH HHS R56 DK068634
6 · The paper itself

Abstract

Jarid2/Jumonji critically regulates developmental processes including cardiovascular development. Jarid2 knock-out mice exhibit cardiac defects including hypertrabeculation with noncompaction of the ventricular wall. However, molecular mechanisms underlying Jarid2-mediated cardiac development remain unknown. To determine the cardiac lineage-specific roles of Jarid2, we generated myocardial, epicardial, cardiac neural crest, or endothelial conditional Jarid2 knock-out mice using Cre-loxP technology. Only mice with an endothelial deletion of Jarid2 recapitulate phenotypic defects observed in whole body mutants including hypertrabeculation and noncompaction of the ventricle. To identify potential targets of Jarid2, combinatorial approaches using microarray and candidate gene analyses were employed on Jarid2 knock-out embryonic hearts. Whole body or endothelial deletion of Jarid2 leads to increased endocardial Notch1 expression in the developing ventricle, resulting in increased Notch1-dependent signaling to the adjacent myocardium. Using quantitative chromatin immunoprecipitation analysis, Jarid2 was found to occupy a specific region on the endogenous Notch1 locus. We propose that failure to properly regulate Notch signaling in Jarid2 mutants likely leads to the defects in the developing ventricular chamber. The identification of Jarid2 as a potential regulator of Notch1 signaling has broad implications for many cellular processes including development, stem cell maintenance, and tumor formation.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsFemaleHeartIn Situ HybridizationMaleMiceMice, KnockoutModels, GeneticMyocardiumNerve Tissue ProteinsOligonucleotide Array Sequence AnalysisPolycomb Repressive Complex 2Receptor, Notch1Transcription, GeneticJarid2 protein, mouseNerve Tissue ProteinsNotch1 protein, mousePolycomb Repressive Complex 2Receptor, Notch1

Identifiers

PMID21402699
PMCPMC3089562
OpenAlexW2009691901

What OpenQuestion holds

Textmetadata
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.