Evidence map›Paper›PMID 25183010›Full record

ArticleThe Journal of biological chemistry2014

Induction of the unfolded protein response by constitutive G-protein signaling in rod photoreceptor cells.

Tian Wang, Jeannie Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Dark continuous noise from mutant G90D-rhodopsin predominantly underlies congenital stationary night blindness.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Review
  5. Arrestin Facilitates Rhodopsin DephosphorylationThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Dark noise and retinal degeneration from D190N-rhodopsin.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Tian WangFrom the Program in Genetic, Molecular and Cellular Biology and the Zilkha Neurogenetic Institute, Department of Cell & Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, California 90089.
Jeannie Chenthe Zilkha Neurogenetic Institute, Department of Cell & Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, California 90089 jeannie@usc.edu.
University of Southern California · US

Funding

Phototransduction in health and diseaseR01EY012155 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Jeannie Chen · 1998 to 2026
$11.8M
VISION RESEARCHP30EY003040 · NEI · DOHENY EYE INSTITUTE · PI SUN, DEMING · 1985 to 2013
$7.0M
NEI NIH HHS EY03040NEI NIH HHS EY12155NEI NIH HHS P30 EY003040NEI NIH HHS R01 EY012155
6 · The paper itself

Abstract

Phototransduction is a G-protein signal transduction cascade that converts photon absorption to a change in current at the plasma membrane. Certain genetic mutations affecting the proteins in the phototransduction cascade cause blinding disorders in humans. Some of these mutations serve as a genetic source of "equivalent light" that activates the cascade, whereas other mutations lead to amplification of the light response. How constitutive phototransduction causes photoreceptor cell death is poorly understood. We showed that persistent G-protein signaling, which occurs in rod arrestin and rhodopsin kinase knock-out mice, caused a rapid and specific induction of the PERK pathway of the unfolded protein response. These changes were not observed in the cGMP-gated channel knock-out rods, an equivalent light condition that mimics light-stimulated channel closure. Thus transducin signaling, but not channel closure, triggers rapid cell death in light damage caused by constitutive phototransduction. Additionally, we show that in the albino light damage model cell death was not associated with increase in global protein ubiquitination or unfolded protein response induction. Taken together, these observations provide novel mechanistic insights into the cell death pathway caused by constitutive phototransduction and identify the unfolded protein response as a potential target for therapeutic intervention.

Indexed as

Unfolded Protein ResponseAnimalsArrestinsbeta-ArrestinsCell DeathCell SurvivalCyclic Nucleotide-Gated Cation ChannelsEndoplasmic Reticulum StressG-Protein-Coupled Receptor Kinase 1GTP-Binding Protein alpha SubunitsGTP-Binding ProteinsLightLight Signal TransductionMiceMice, Inbred BALB CMice, Inbred C57BLArrestinsbeta-ArrestinsCngb1 protein, mouseCyclic Nucleotide-Gated Cation ChannelsGnat1 protein, mouseG-Protein-Coupled Receptor Kinase 1Grk1 protein, mouseGTP-Binding Protein alpha SubunitsGTP-Binding ProteinsNerve Tissue ProteinsRhodopsinTransducinG-proteinLight DamagePhotoreceptorRetinal DegenerationRhodopsinUnfolded Protein Response (UPR)

Identifiers

PMID25183010
PMCPMC4200281
OpenAlexW2072402974

What OpenQuestion holds

Textmetadata
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.