Evidence map›Paper›PMID 17108167›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Stable rhodopsin/arrestin complex leads to retinal degeneration in a transgenic mouse model of autosomal dominant retinitis pigmentosa.

Jiayan Chen, Guang Shi, Francis A Concepcion, Guifu Xie, Daniel Oprian, Jeannie Chen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

46 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Aggregation of the Constitutively Active K296E Rhodopsin Mutant Contributes to Retinal Degeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  3. Article
  4. Article
  5. Arrestin Facilitates Rhodopsin DephosphorylationThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  6. Article
  7. Review
  8. Dark noise and retinal degeneration from D190N-rhodopsin.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Biochemical Measurements of Free Opsin in Macular Degeneration Eyes: Examining the 11-Transactions of the American Ophthalmological Society · 2017
    Review
  14. Article
  15. Article
  16. Effect of Rhodopsin Phosphorylation on Dark Adaptation in Mouse Rods.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Jiayan ChenZilkha Neurogenetic Institute, University of Southern California, Los Angeles, California 90033, USA.
Guang Shi
Francis A Concepcion
Guifu Xie
Daniel Oprian
Jeannie Chen
University of Southern California · USBrandeis University · US

Funding

Phototransduction in health and diseaseR01EY012155 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Jeannie Chen · 1998 to 2026
$11.8M
STRUCTURE/FUNCTION STUDIES OF RHODOPSINR01EY007965 · NEI · BRANDEIS UNIVERSITY · PI OPRIAN, DANIEL D · 1989 to 2017
$6.2M
NEI NIH HHS EY12155NEI NIH HHS R01 EY007965NEI NIH HHS R01 EY012155
6 · The paper itself

Abstract

Over 100 rhodopsin mutation alleles have been associated with autosomal dominant retinitis pigmentosa (ADRP). These mutations appear to cause photoreceptor cell death through diverse molecular mechanisms. We show that K296E, a rhodopsin mutation associated with ADRP, forms a stable complex with arrestin that is toxic to mouse rod photoreceptors. This cell death pathway appears to be conserved from flies to mammals. A genetics approach to eliminate arrestin unmasked the constitutive activity of K296E and caused photoreceptor cell death through a transducin-dependent mechanism that is similar to light damage. Expressing K296E in the arrestin/transducin double knock-out background prevented transducin signaling and led to substantially improved retinal morphology but did not fully prevent cell death caused by K296E. The adverse effect of K296E in the arrestin/transducin knock-out background can be mimicked by constant exposure to low light. Furthermore, we found that arrestin binding causes K296E to mislocalize to the wrong cellular compartment. Accumulation of stable rhodopsin/arrestin complex in the inner segment may be an important mechanism for triggering the cell death pathway in the mammalian photoreceptor cell.

Indexed as

AnimalsArrestinCell CompartmentationCell DeathChromosome DisordersDisease Models, AnimalFemaleGenes, DominantHumansLightMacromolecular SubstancesMaleMiceMice, KnockoutMice, TransgenicMutationArrestinMacromolecular SubstancesRhodopsinTransducin

Identifiers

PMID17108167
PMCPMC6674877
OpenAlexW1995155011

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.