Evidence map›Paper›PMID 24983376›Full record

ArticlePloS one2014

Cryptorchidism and infertility in rats with targeted disruption of the Adamts16 locus.

Shakila Abdul-Majeed, Blair Mell, Surya M Nauli, Bina Joe

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. A nonsense mutation in mouse Adamtsl2 causes uterine hypoplasia and an irregular estrous cycle.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Metalloproteases in gonad formation and ovulation.General and comparative endocrinology · 2021
    Review
  9. Hyalectanase Activities by the ADAMTS Metalloproteases.International journal of molecular sciences · 2021
    Review
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  11. Review
  12. Review
  13. Article
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  16. Article
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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 1 institution in 1 country.

Shakila Abdul-MajeedCenter for Hypertension and Personalized Medicine, Program in Physiological Genomics, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, United States of America.
Blair MellCenter for Hypertension and Personalized Medicine, Program in Physiological Genomics, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, United States of America.
Surya M NauliDepartment of Pharmacology, University of Toledo College of Pharmacy, Toledo, Ohio, United States of America.
Bina JoeCenter for Hypertension and Personalized Medicine, Program in Physiological Genomics, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, United States of America.
University of Toledo · US

Funding

Genetics of HypertensionR01HL020176 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI JOE, BINA · 1985 to 2017
$8.1M
Innovative Models for Mechanistic Studies of Novel Hypertension GenesR01HL112641 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI JOE, BINA · 2012 to 2016
$3.3M
BIOCHEMISTRY AND GENETICS OF HYPERTENSIONR37HL020176 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI RAPP, JOHN P · 1993 to 2002
$1.6M
NHLBI NIH HHS R01 HL020176NHLBI NIH HHS R01 HL112641NHLBI NIH HHS R37 HL020176
6 · The paper itself

Abstract

A Disintegrin And Metalloproteinase with ThromboSpondin motifs16 (ADAMTS-16) is a member of a family of metalloproteinases. Using a novel zinc-finger nuclease based gene-edited rat model harboring a targeted mutation of the Adamts16 locus, we previously reported this gene to be linked to blood pressure regulation. Here we document our observation with this model that Adamts16 is essential for normal development of the testis. Absence of Adamts16 in the homozygous Adamts16mutant males resulted in cryptorchidism and male sterility. Heterozygous Adamts16mutant males were normal, indicating that this is a recessive trait. Testes of homozygous Adamts16mutant males were significantly smaller with significant histological changes associated with the lack of sperm production. Temporal histological assessments of the testis demonstrated that the seminiferous tubules did not support active spermatogenesis, but progressively lost germ cells, accumulated vacuoles and did not have any sperm. These observations, taken together with our previous report of renal abnormalities observed with the same Adamts16mutant rats, suggest an important mechanistic link between Adamts16 and the functioning of the male genitourinary system.

Indexed as

Genetic LociMutationSpermatogenesisADAM ProteinsAnimalsCryptorchidismInfertility, MaleKidneyMaleRatsADAM Proteins

Identifiers

PMID24983376
PMCPMC4077762
OpenAlexW2082857203

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.