Evidence map›Paper›PMID 29463953›Full record

ArticleMolecular vision2018

Autosomal dominant retinitis pigmentosa rhodopsin mutant Q344X drives specific alterations in chromatin complex gene transcription.

Katie L Bales, Lara Ianov, Andrew J Kennedy, J David Sweatt, Alecia K Gross

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Current Advancements in Mouse Models of Retinal Disease.Advances in experimental medicine and biology · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. 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

5 authors at 4 institutions in 1 country.

Katie L BalesSchool of Optometry, Department of Optometry and Vision Science, University of Alabama at Birmingham, Birmingham, AL.
Lara IanovSchool of Medicine, Civitan International Research Center, University of Alabama at Birmingham, AL.
Andrew J KennedyDepartment of Chemistry and Biochemistry, Bates College, Lewiston, ME.
J David SweattSchool of Medicine, Department of Pharmacology, Vanderbilt University, TN.
Alecia K GrossSchool of Optometry, Department of Optometry and Vision Science, University of Alabama at Birmingham, Birmingham, AL.
Civitan International · USBates College · USUniversity of Alabama at Birmingham · USVanderbilt University · US

Funding

Biochemical Mechanisms of Neural PlasticityR01MH057014 · NIMH · VANDERBILT UNIVERSITY · PI WINDER, DANNY G. · 1996 to 2019
$9.3M
Rhodopsin Trafficking and Retinal DegenerationsR01EY019311 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GROSS, ALECIA K · 2008 to 2012
$1.9M
NEI NIH HHS R01 EY019311NIMH NIH HHS R01 MH057014
6 · The paper itself

Abstract

Purpose: Epigenetic and transcriptional mechanisms have been shown to contribute to long-lasting functional changes in adult neurons. The purpose of this study was to identify any such modifications in diseased retinal tissues from a mouse model of rhodopsin mutation-associated autosomal dominant retinitis pigmentosa (ADRP), Q344X, relative to age-matched wild-type (WT) controls. Methods: We performed RNA sequencing (RNA-seq) at poly(A) selected RNA to profile the transcriptional patterns in 3-week-old ADRP mouse model rhodopsin Q344X compared to WT controls. Differentially expressed genes were determined by DESeq2 using the Benjamini & Hochberg p value adjustment and an absolute log Results: We observed significant differential expression in 2151 genes in the retina of Q344X mice compared to WT controls, including downregulation in the potassium channel gene, Conclusions: These findings provide evidence that transcriptomic alterations occur in the ADRP mouse model rhodopsin Q344X retina and that these processes may contribute to the dysfunction and neurodegeneration seen in this animal model.

Indexed as

Amino Acid SubstitutionTranscription, GeneticAnimalsChromatinChromosome DisordersFemaleGene Expression ProfilingGene Knock-In TechniquesGenes, DominantHistone DeacetylasesHistonesHumansMaleMiceMice, TransgenicMutationChromatinH1f8 protein, mouseHdac9 protein, mouseHistone DeacetylasesHistonesKcnv2 protein, mousePotassium Channels, Voltage-GatedProtein IsoformsRepressor ProteinsRhodopsin

Identifiers

PMID29463953
PMCPMC5815338
OpenAlexW2788329690

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.