Evidence map›Paper›PMID 29262782›Full record

ArticleBMC genomics2017

Genes uniquely expressed in human growth plate chondrocytes uncover a distinct regulatory network.

Bing Li, Karthika Balasubramanian, Deborah Krakow, Daniel H Cohn

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

Article in BMC genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Role of non‑coding RNAs in cartilage endplate (Review).Experimental and therapeutic medicine · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Targeting defective proteostasis in the collagenopathies.Current opinion in chemical biology · 2019
    Review
  11. Review
  12. Review
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 1 institution in 1 country.

Bing LiDepartment of Molecular, Cell, and Developmental Biology, University of California Los Angeles, CA, Los Angeles, USA.
Karthika BalasubramanianDepartment of Molecular, Cell, and Developmental Biology, University of California Los Angeles, CA, Los Angeles, USA.
Deborah KrakowDepartment of Orthopaedic Surgery, David Geffen School of Medicine at the University of California Los Angeles, CA, Los Angeles, USA.
Daniel H CohnDepartment of Molecular, Cell, and Developmental Biology, University of California Los Angeles, CA, Los Angeles, USA. dcohn@mcdb.ucla.edu.ORCID http://orcid.org/0000-0003-0388-4457
University of California, Los Angeles · US

Funding

Exome sequencing in the skeletal dysplasiasR01AR062651 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COHN, DANIEL H · 2013 to 2017
$1.7M
Unraveling the mechanisms of prenatal-onset disorders affecting the skeletonR01AR066124 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KRAKOW, DEBORAH · 2014 to 2018
$1.7M
National Institute of Arthritis and Musculoskeletal and Skin Diseases RO1AR062651National Institute of Arthritis and Musculoskeletal and Skin Diseases RO1AR066124NIAMS NIH HHS R01 AR062651NIAMS NIH HHS R01 AR066124
6 · The paper itself

Abstract

backgroundChondrogenesis is the earliest stage of skeletal development and is a highly dynamic process, integrating the activities and functions of transcription factors, cell signaling molecules and extracellular matrix proteins. The molecular mechanisms underlying chondrogenesis have been extensively studied and multiple key regulators of this process have been identified. However, a genome-wide overview of the gene regulatory network in chondrogenesis has not been achieved.

resultsIn this study, employing RNA sequencing, we identified 332 protein coding genes and 34 long non-coding RNA (lncRNA) genes that are highly selectively expressed in human fetal growth plate chondrocytes. Among the protein coding genes, 32 genes were associated with 62 distinct human skeletal disorders and 153 genes were associated with skeletal defects in knockout mice, confirming their essential roles in skeletal formation. These gene products formed a comprehensive physical interaction network and participated in multiple cellular processes regulating skeletal development. The data also revealed 34 transcription factors and 11,334 distal enhancers that were uniquely active in chondrocytes, functioning as transcriptional regulators for the cartilage-selective genes.

conclusionsOur findings revealed a complex gene regulatory network controlling skeletal development whereby transcription factors, enhancers and lncRNAs participate in chondrogenesis by transcriptional regulation of key genes. Additionally, the cartilage-selective genes represent candidate genes for unsolved human skeletal disorders.

Indexed as

Gene Regulatory NetworksCartilageChondrocytesChondrogenesisEnhancer Elements, GeneticFetusGene Expression ProfilingGrowth PlateHumansProtein Interaction MapsRNA, Long NoncodingRNA, Long NoncodingCartilageChondrocyteGene expressionHumanlncRNARNA-seqSkeletal dysplasia

Identifiers

PMID29262782
PMCPMC5738906
OpenAlexW2779580699

What OpenQuestion holds

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Registered trials

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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.