Evidence map›Paper›PMID 27750040›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2017

TNFa knockdown in the retina promotes cone survival in a mouse model of autosomal dominant retinitis pigmentosa.

Tapasi Rana, Pravallika Kotla, Roderick Fullard, Marina Gorbatyuk

Abstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Immunology of Retinitis Pigmentosa and Gene Therapy-Associated Uveitis.Cold Spring Harbor perspectives in medicine · 2024
    Review
  3. Review
  4. Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023
    Review
  5. Mechanism of Cone Degeneration in Retinitis Pigmentosa.Cellular and molecular neurobiology · 2023
    Review
  6. GADD34 Ablation Exacerbates Retinal Degeneration in P23H RHO Mice.International journal of molecular sciences · 2022
    Article
  7. Review
  8. Review
  9. Article
  10. Retinal Inflammation, Cell Death and Inherited Retinal Dystrophies.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Neurodegeneration: Keeping ATF4 on a Tight Leash.Frontiers in cellular neuroscience · 2017
    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

4 authors at 1 institution in 1 country.

Tapasi RanaUniversity of Alabama at Birmingham, Department of Optometry and Vision Science, United States.
Pravallika KotlaUniversity of Alabama at Birmingham, Department of Optometry and Vision Science, United States.
Roderick FullardUniversity of Alabama at Birmingham, Department of Optometry and Vision Science, United States.
Marina GorbatyukUniversity of Alabama at Birmingham, Department of Optometry and Vision Science, United States. Electronic address: mgortk@uab.edu.
University of Alabama at Birmingham · US

Funding

Visual Phenotyping CoreP30EY003039 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Paul Douglas Gamlin · 1985 to 2026
$16.9M
Unfolded Protein Response as a Therapeutic Target for ADRP Animal ModelsR01EY020905 · NEI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI GORBATYUK, MARINA · 2010 to 2014
$1.3M
NEI NIH HHS P30 EY003039NEI NIH HHS R01 EY020905
6 · The paper itself

Abstract

Expression of T17M rhodopsin (T17M) in rods activates the Unfolded Protein Response (UPR) and leads to the development of autosomal dominant retinitis pigmentosa (adRP). The rod death occurs in adRP retinas prior to cone photoreceptor death, so the mechanism by which cone photoreceptors die remains unclear. Therefore, the goal of the study was to verify whether UPR in rods induces TNFa-mediated signaling to the cones and to determine whether the TNFa deficit could prevent adRP cone cell death. Primary rod photoreceptors and cone-derived 661W cells transfected with siRNA against TNFa were treated with tunicamycin to mimic activation of UPR in T17M retinas expressing normal and reduced TNFa levels. The 661W cells were then exposed to recombinant TNFa to evaluate cell viability. In vivo, the role of TNFa was assessed in T17M TNFa

Indexed as

Gene Knockdown TechniquesAnimalsCells, CulturedCell SurvivalFemaleInflammationMaleMiceMice, Inbred C57BLRetinal Cone Photoreceptor CellsRetinal Rod Photoreceptor CellsRetinitis PigmentosaTumor Necrosis Factor-alphaUnfolded Protein ResponseTumor Necrosis Factor-alphaCone survivalRetinal degenerationT17M rhodopsinTransgenic miceTumor necrosis factorUnfolded protein response

Identifiers

PMID27750040
PMCPMC6056179
OpenAlexW2532951275

What OpenQuestion holds

Textmetadata
LicenceTDM
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.