Evidence map›Paper›PMID 33022452›Full record

ArticleBone2021

Mesenchyme-specific loss of Dot1L histone methyltransferase leads to skeletal dysplasia phenotype in mice.

Pearl A Sutter, Sangita Karki, Ilan Crawley, Vijender Singh, Kathrin M Bernt, David W Rowe, Stephen J Crocker, Dashzeveg Bayarsaihan, Rosa M Guzzo

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bone, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. DOT-1.1 (DOT1L) deficiency inBBA advances · 2023
    Article
  5. Article
  6. Connecting the DOTs on Cell Identity.Frontiers in cell and developmental biology · 2022
    Review
  7. Review
  8. 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 4 institutions in 1 country.

Pearl A SutterDepartment of Neuroscience, School of Medicine, University of Connecticut Health, Farmington, CT, United States of America.
Sangita KarkiDepartment of Neuroscience, School of Medicine, University of Connecticut Health, Farmington, CT, United States of America.
Ilan CrawleyDepartment of Neuroscience, School of Medicine, University of Connecticut Health, Farmington, CT, United States of America.
Vijender SinghBioinformatics, University of Connecticut, Storrs, CT, United States of America.
Kathrin M BerntDivision of Pediatric Oncology, Children's Hospital of Philadelphia, Perelman School of Medicine at the University of Pennsylvania and Abramson Cancer Center, Philadelphia, PA, United States of America.
David W RoweDepartment of Reconstructive Sciences, School of Dental Medicine, University of Connecticut Health, Farmington, CT, United States of America; Center for Regenerative Medicine and Skeletal Development, Farmington, CT, United States of America.
Stephen J CrockerDepartment of Neuroscience, School of Medicine, University of Connecticut Health, Farmington, CT, United States of America.
Dashzeveg BayarsaihanDepartment of Reconstructive Sciences, School of Dental Medicine, University of Connecticut Health, Farmington, CT, United States of America; Center for Regenerative Medicine and Skeletal Development, Farmington, CT, United States of America.
Rosa M GuzzoDepartment of Neuroscience, School of Medicine, University of Connecticut Health, Farmington, CT, United States of America. Electronic address: guzzo@uchc.edu.
UConn Health · USCenter for Neuroscience and Regenerative Medicine · USUniversity of Connecticut · USUniversity of Pennsylvania · US

Funding

Skeletal Phenotyping of Heterozygotes from IMPC Embryonic Lethal LinesR01HD098636 · NICHD · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MAYE, PETER, ROWE, DAVID W. · 2019 to 2023
$2.8M
Understanding how Dot1L activity in the growth plate regulates skeletal growthR03HD097426 · NICHD · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI GUZZO, ROSARIA M. · 2019 to 2020
$164k
NICHD NIH HHS R01 HD098636NICHD NIH HHS R03 HD097426
6 · The paper itself

Abstract

Chromatin modifying enzymes play essential roles in skeletal development and bone maintenance, and deregulation of epigenetic mechanisms can lead to skeletal growth and malformation disorders. Here, we report a novel skeletal dysplasia phenotype in mice with conditional loss of Disruptor of telomeric silencing 1-like (Dot1L) histone methyltransferase in limb mesenchymal progenitors and downstream descendants. Phenotypic characterizations of mice with Dot1L inactivation by Prrx1-Cre (Dot1L-cKO

Indexed as

ChondrocytesMesodermAnimalsHistone-Lysine N-MethyltransferaseHistone MethyltransferasesMicePhenotypeX-Ray MicrotomographyDot1l protein, mouseHistone-Lysine N-MethyltransferaseHistone MethyltransferasesCartilageDot1LGrowth plateSkeletal dysplasia

Identifiers

PMID33022452
PMCPMC7744341
OpenAlexW3090718378

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.