Evidence map›Paper›PMID 31848143›Full record

ArticleDisease models & mechanisms2019

Regulation of terminal hypertrophic chondrocyte differentiation in

Zhaoyang Liu, Janani Ramachandran, Steven A Vokes, Ryan S Gray

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

Article in Disease models & mechanisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 19 citations in OpenAlex.

  1. The G protein-coupled receptor ADGRG6 maintains mouse growth plate homeostasis through IHH signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
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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

4 authors at 2 institutions in 1 country.

Zhaoyang LiuDepartment of Pediatrics, Dell Pediatric Research Institute, 1400 Barbara Jordan Blvd, The University of Texas at Austin, Dell Medical School, Austin, TX 78723, USA.
Janani RamachandranDepartment of Molecular Biosciences, 2500 Speedway, The University of Texas at Austin, Austin, TX 78712, USA.
Steven A VokesDepartment of Molecular Biosciences, 2500 Speedway, The University of Texas at Austin, Austin, TX 78712, USA.
Ryan S GrayDepartment of Pediatrics, Dell Pediatric Research Institute, 1400 Barbara Jordan Blvd, The University of Texas at Austin, Dell Medical School, Austin, TX 78723, USA ryan.gray@austin.utexas.edu.ORCID 0000-0001-9668-6497
Dell Children's Medical Center of Central Texas · USThe University of Texas at Austin · US

Funding

Cis-regulatory circuitry underlying Hedgehog mediated limb developmentR01HD073151 · NICHD · UNIVERSITY OF TEXAS AT AUSTIN · PI Steven Alexander Vokes · 2012 to 2026
$5.1M
Towards a Mechanistic Undestanding of Adolscent Idiopathic ScoliosisR01AR072009 · NIAMS · UNIVERSITY OF TEXAS AT AUSTIN · PI Ryan Scott Gray · 2017 to 2026
$3.9M
Investigating the Role of Gpr126 in cartilage for Intervertebral Disc and Spine HomeostasisF32AR073648 · NIAMS · UNIVERSITY OF TEXAS AT AUSTIN · PI LIU, ZHAOYANG · 2018 to 2020
$197k
Elucidating the Cellular and Molecular Mechanisms of Late-Onset ScoliosisF32AR063001 · NIAMS · WASHINGTON UNIVERSITY · PI GRAY, RYAN SCOTT · 2012 to 2014
$163k
NIAMS NIH HHS F32 AR063001NIAMS NIH HHS F32 AR073648NIAMS NIH HHS R01 AR072009NICHD NIH HHS R01 HD073151
6 · The paper itself

Abstract

Idiopathic scoliosis (IS) is the most common type of musculoskeletal defect affecting children worldwide, and is classified by age of onset, location and degree of spine curvature. Although rare, IS with onset during infancy is the more severe and rapidly progressive form of the disease, associated with increased mortality due to significant respiratory compromise. The pathophysiology of IS, in particular for infantile IS, remains elusive. Here, we demonstrate the role of PRMT5 in the infantile IS phenotype in mouse. Conditional genetic ablation of PRMT5 in osteochondral progenitors results in impaired terminal hypertrophic chondrocyte differentiation and asymmetric defects of endochondral bone formation in the perinatal spine. Analysis of these several markers of endochondral ossification revealed increased type X collagen (COLX) and

Indexed as

Gene Expression Regulation, DevelopmentalAllelesAnimalsBone Morphogenetic Protein 4CartilageCell DifferentiationCell ProliferationChondrocytesChondrogenesisCore Binding Factor Alpha 1 SubunitCrosses, GeneticGene DeletionHedgehog ProteinsHomeostasisMatrix Metalloproteinase 13MiceBmp4 protein, mouseBone Morphogenetic Protein 4Core Binding Factor Alpha 1 SubunitHedgehog Proteinsihh protein, mouseMatrix Metalloproteinase 13Mmp13 protein, mousePrmt5 protein, mouseProtein-Arginine N-MethyltransferasesRunx2 protein, mouseChondrocyte terminal differentiationEndochondral ossificationInfantile scoliosisPRMT5

Identifiers

PMID31848143
PMCPMC6955203
OpenAlexW2996170301

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.