Evidence map›Paper›PMID 30779420›Full record

ReviewAmerican journal of medical genetics. Part C, Seminars in medical genetics2019

The mouse as a model of fundamental concepts related to Turner syndrome.

Arthur P Arnold

Abstract readReview
In one paragraph

Review in American journal of medical genetics. Part C, Seminars in medical genetics, 2019. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. A Review of Recent Developments in Turner Syndrome Research.Journal of cardiovascular development and disease · 2021
    Review
  7. Article
  8. 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

1 author.

Arthur P ArnoldDepartment of Integrative Biology and Physiology, Laboratory of Neuroendocrinology of the Brain Research Institute, University of California, Los Angeles, California.ORCID 0000-0002-9908-9767

Funding

Center for Clinical and Translational Sciences (CCTS)UL1TR000371 · NCATS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCPHERSON, DAVID D · 2012 to 2016
$13.4M
Sex Chromosome Effects on Neural DevelopmentR01NS043196 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P · 2003 to 2013
$3.4M
Genetic Mechanisms in Klinefelter Syndrome-Related BehaviorsR01HD076125 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P, JENTSCH, J. DAVID · 2014 to 2018
$2.3M
Sex differences in obesity and metabolic diseaseR01DK083561 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P, CHEN, XUQI · 2010 to 2014
$1.6M
Epigenetic regulation of myocardial ischemia/reperfusion injury by X chromosomeR01HL131182 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P, EGHBALI, MANSOUREH · 2016 to 2019
$1.5M
Discriminating sex chromosome and hormonal effects on brain sexual dimorphismsR21HD090637 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P, MACKENZIE-GRAHAM, ALLAN JAMES · 2017 to 2018
$428k
X chromosome dosage and metabolic diseaseR56DK083561 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P, REUE, KAREN · 2016 to 2016
$154k
National Institute of Child Health and Human Development HD076125National Institute of Child Health and Human Development HD090637NCATS NIH HHS UL1 TR000371NHLBI NIH HHS HL131182NHLBI NIH HHS R01 HL131182NICHD NIH HHS R01 HD076125NICHD NIH HHS R21 HD090637NIDDK NIH HHS DK083561NIDDK NIH HHS R01 DK083561NIDDK NIH HHS R56 DK083561NINDS NIH HHS NS043196NINDS NIH HHS R01 NS043196
6 · The paper itself

Abstract

Although XO mice do not show many of the overt phenotypic features of Turner syndrome (TS; 45,X or XO), mice and humans share different classes of genes on the X chromosome that are more or less likely to cause TS phenotypes. Based on the evolutionary history of the sex chromosomes, and the pattern of dosage balancing among sex chromosomal and autosomal genes in functional gene networks, it is possible to prioritize types of X genes for study as potential causes of features of TS. For example, X-Y gene pairs are among the most interesting because of the convergent effects of X and Y genes that both are likely to prevent the effects of TS in XX and XY individuals. Many of the high-priority genes are shared by mouse and human X chromosomes, but are easier to study in genetically tractable mouse models. Several mouse models, used primarily for the study of sex differences in physiology and disease, also produce XO mice that can be investigated to understand the effects of X monosomy. Using these models will lead to the identification of specific X genes that make a difference when present in one or two copies. These studies will help to achieve a better appreciation of the contribution of these specific X genes to the syndromic features of TS.

Indexed as

Genes, X-LinkedAnimalsDisease Models, AnimalFemaleHumansMiceMonosomySex CharacteristicsTurner Syndromefour core genotypessex chromosome aneuploidyTurner syndrome

Identifiers

PMID30779420
PMCPMC7532839

What OpenQuestion holds

Textmetadata
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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.