Evidence map›Paper›PMID 26483638›Full record

ArticleFrontiers in cellular neuroscience2015

Increased phosphorylation of Cx36 gap junctions in the AII amacrine cells of RD retina.

Elena Ivanova, Christopher W Yee, Botir T Sagdullaev

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Inhibitory Circuits Can Restore OFF Pathway Responses in Retinal Prostheses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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  9. Network Architecture of Gap Junctional Coupling among Parallel Processing Channels in the Mammalian Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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  19. Retinal remodeling in human retinitis pigmentosa.Experimental eye research · 2016
    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

3 authors at 2 institutions in 1 country.

Elena IvanovaDepartments of Ophthalmology and Neurology, Burke Medical Research Institute, Weill Medical College of Cornell University White Plains, NY, USA.
Christopher W YeeDepartments of Ophthalmology and Neurology, Burke Medical Research Institute, Weill Medical College of Cornell University White Plains, NY, USA.
Botir T SagdullaevDepartments of Ophthalmology and Neurology, Burke Medical Research Institute, Weill Medical College of Cornell University White Plains, NY, USA.
Cornell University · USBurke Medical Research Institute · US

Funding

Retinal neural processing during retinal degenerative diseasesR01EY020535 · NEI · WINIFRED MASTERSON BURKE MED RES INST · PI SAGDULLAEV, BOTIR T. · 2010 to 2014
$2.4M
NEI NIH HHS R01 EY020535
6 · The paper itself

Abstract

Retinal degeneration (RD) encompasses a family of diseases that lead to photoreceptor death and visual impairment. Visual decline due to photoreceptor cell loss is further compromised by emerging spontaneous hyperactivity in inner retinal cells. This aberrant activity acts as a barrier to signals from the remaining photoreceptors, hindering therapeutic strategies to restore light sensitivity in RD. Gap junctions, particularly those expressed in AII amacrine cells, have been shown to be integral to the generation of aberrant activity. It is unclear whether gap junction expression and coupling are altered in RD. To test this, we evaluated the expression and phosphorylation state of connexin36 (Cx36), the gap junction subunit predominantly expressed in AII amacrine cells, in two mouse models of RD, rd10 (slow degeneration) and rd1 (fast degeneration). Using Ser293-P antibody, which recognizes a phosphorylated form of connexin36, we found that phosphorylation of connexin36 in both slow and fast RD models was significantly greater than in wildtype controls. This elevated phosphorylation may underlie the increased gap junction coupling of AII amacrine cells exhibited by RD retina.

Indexed as

AII amacrine cellsgap junctionshyperactivityoscillationsphosphorylationretinal degenerationspontaneous activity

Identifiers

PMID26483638
PMCPMC4589668
OpenAlexW2098834080

What OpenQuestion holds

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LicenceCC BY
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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.