Evidence map›Paper›PMID 23922682›Full record

ArticlePloS one2013

Loss of NAC1 expression is associated with defective bony patterning in the murine vertebral axis.

Kai Lee Yap, Polina Sysa-Shah, Brad Bolon, Ren-Chin Wu, Min Gao, Alice L Herlinger, Fengying Wang, Francesco Faiola, David Huso, Kathleen Gabrielson and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Development of a Novel 11-Gene Signature Related to Immune Subtypes for FibromyalgiaEndocrine, metabolic & immune disorders drug targets · 2026
    Article
  2. Article
  3. Nacc1 Mutation in Mice Models Rare Neurodevelopmental Disorder with Underlying Synaptic Dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  4. Knockout mouse models as a resource for the study of rare diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Article
  5. Review
  6. Article
  7. A New Case ofFrontiers in pediatrics · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Identification of the NAC1-regulated genes in ovarian cancer.The American journal of pathology · 2014
    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

13 authors at 4 institutions in 2 countries.

Kai Lee YapDepartment of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland, United States of America.
Polina Sysa-Shah
Brad Bolon
Ren-Chin Wu
Min Gao
Alice L Herlinger
Fengying Wang
Francesco Faiola
David Huso
Kathleen Gabrielson
Tian-Li Wang
Jianlong Wang
Ie-Ming Shih
Johns Hopkins University · USIcahn School of Medicine at Mount Sinai · USThe Ohio State University · USUniversidade Federal do Espírito Santo · BR

Funding

Molecular Diagnostics for Malignant EffusionR01CA103937 · NCI · JOHNS HOPKINS UNIVERSITY · PI SHIH, IE-MING · 2004 to 2012
$2.7M
Characterizing Notch3 Signaling in Ovarian CancerR01CA148826 · NCI · JOHNS HOPKINS UNIVERSITY · PI WANG, TIAN-LI · 2011 to 2015
$1.7M
NCI NIH HHS R01 CA103937NCI NIH HHS R01CA103937NCI NIH HHS R01 CA148826NCI NIH HHS R01CA148826
6 · The paper itself

Abstract

NAC1 encoded by NACC1 is a member of the BTB/POZ family of proteins and participates in several pathobiological processes. However, its function during tissue development has not been elucidated. In this study, we compared homozygous null mutant Nacc1(-/-) and wild type Nacc1(+/+) mice to determine the consequences of diminished NAC1 expression. The most remarkable change in Nacc1(-/-) mice was a vertebral patterning defect in which most knockout animals exhibited a morphological transformation of the sixth lumbar vertebra (L6) into a sacral identity; thus, the total number of pre-sacral vertebrae was decreased by one (to 25) in Nacc1(-/-) mice. Heterozygous Nacc1(+/-) mice had an increased tendency to adopt an intermediate phenotype in which L6 underwent partial sacralization. Nacc1(-/-) mice also exhibited non-closure of the dorsal aspects of thoracic vertebrae T10-T12. Chondrocytes from Nacc1(+/+) mice expressed abundant NAC1 while Nacc1(-/-) chondrocytes had undetectable levels. Loss of NAC1 in Nacc1(-/-) mice was associated with significantly reduced chondrocyte migratory potential as well as decreased expression of matrilin-3 and matrilin-4, two cartilage-associated extracellular matrix proteins with roles in the development and homeostasis of cartilage and bone. These data suggest that NAC1 participates in the motility and differentiation of developing chondrocytes and cartilaginous tissues, and its expression is necessary to maintain normal axial patterning of murine skeleton.

Indexed as

Body PatterningAllelesAnimalsBreedingCartilageCell MovementCell ProliferationChondrocytesCrosses, GeneticEmbryo, MammalianFemaleGenotypeLumbar VertebraeMaleMatrilin ProteinsMiceMatrilin ProteinsNacc1 protein, mouseNerve Tissue ProteinsRepressor Proteins

Identifiers

PMID23922682
PMCPMC3724875
OpenAlexW1983192202

What OpenQuestion holds

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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.