Evidence map›Paper›PMID 11178107›Full record

ArticleBMC genetics2001

Genetic modification of glaucoma associated phenotypes between AKXD-28/Ty and DBA/2J mice.

M G Anderson, R S Smith, O V Savinova, N L Hawes, B Chang, A Zabaleta, R Wilpan, J R Heckenlively, M Davisson, S W John

Open access · diamondAbstract readComparative Study
In one paragraph

Article in BMC genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Genetic modifiers and oligogenic inheritance.Cold Spring Harbor perspectives in medicine · 2015
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Manganese-enhanced MRI of the DBA/2J mouse model of hereditary glaucoma.Investigative ophthalmology & visual science · 2008
    Article
  18. Article
  19. Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2007
    Article
  20. Vascular changes in the posterior eye segment of secondary angle-closure glaucoma: cause or consequence?Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2006
    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

10 authors at 2 institutions in 1 country.

M G AndersonThe Howard Hughes Medical Institute, Bar Harbor, Maine, USA. mga@jax.org
R S Smith
O V Savinova
N L Hawes
B Chang
A Zabaleta
R Wilpan
J R Heckenlively
M Davisson
S W John
Jackson Laboratory · USHoward Hughes Medical Institute · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Mouse Models of Human Hereditary Eye DiseasesR01EY007758 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HECKENLIVELY, JOHN R · 1988 to 2007
$3.4M
NCI NIH HHS CA34196NCI NIH HHS P30 CA034196NEI NIH HHS EY07758NEI NIH HHS R01 EY007758
6 · The paper itself

Abstract

backgroundGlaucoma is a common disease but its molecular etiology is poorly understood. It involves retinal ganglion cell death and optic nerve damage that is often associated with elevated intraocular pressure. Identifying genes that modify glaucoma associated phenotypes is likely to provide insights to mechanisms of glaucoma. We previously reported glaucoma in DBA/2J mice caused by recessive alleles at two loci, isa and ipd, that cause iris stromal atrophy and iris pigment dispersion, respectively. A approach for identifying modifier genes is to study the effects of specific mutations in different mouse strains. When the phenotypic effect of a mutation is modified upon its introduction into a new strain, crosses between the parental strains can be used to identify modifier genes. The purpose of this study was to determine if the effects of the DBA/2J derived isa and ipd loci are modified in strain AKXD-28/Ty.

resultsAKXD-28/Ty mice develop glaucoma characterized by intraocular pressure elevation, retinal ganglion loss, and optic nerve excavation. In AKXD-28/Ty, isa causes an iris stromal atrophy phenotype as in DBA/2J. However, the iris pigment dispersion phenotype associated with ipd in DBA/2J does not occur in AKXD-28/Ty. Additionally, a greater severity and speed of retinal and optic nerve damage following intraocular pressure elevation in AKXD-28/Ty compared to DBA/2J mice suggests that AKXD-28/Ty is more susceptible to pressure-induced cell death.

conclusionsThe consequences of the ipd and isa mutations are modified in the AKXD-28/Ty background. These strains provide a resource for the identification of modifier genes that modulate pigment dispersion and susceptibility to pressure-induced cell death.

Indexed as

Genetic Predisposition to DiseaseAnimalsAtrophyFemaleGlaucomaIrisMaleMiceMice, Inbred C57BLMice, Inbred DBAMice, Inbred StrainsMutationOptic Nerve DiseasesPhenotypePigment Epithelium of EyeRetinal Diseases

Identifiers

PMID11178107
PMCPMC29081
OpenAlexW1880717070

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.