Evidence map›Paper›PMID 27995734›Full record

ArticleJournal of cellular and molecular medicine2017

The X-linked juvenile retinoschisis protein retinoschisin is a novel regulator of mitogen-activated protein kinase signalling and apoptosis in the retina.

Karolina Plössl, Bernhard H F Weber, Ulrike Friedrich

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. 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
1.0field-weighted citation impact, top 21% 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, 32 citations in OpenAlex.

  1. Article
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  4. Cells · 2025
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  9. Evaluation of mesenchymal stem cells as anFrontiers in cell and developmental biology · 2024
    Review
  10. A Spontaneous Nonhuman Primate Model of Myopic Foveoschisis.Investigative ophthalmology & visual science · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Retinoschisin and Cardiac Glycoside Crosstalk at the Retinal Na/K-ATPase.Investigative ophthalmology & visual science · 2020
    Article
  17. Article
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Karolina PlösslInstitute of Human Genetics, University of Regensburg, Regensburg, Germany.
Bernhard H F WeberInstitute of Human Genetics, University of Regensburg, Regensburg, Germany.
Ulrike FriedrichInstitute of Human Genetics, University of Regensburg, Regensburg, Germany.
University of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

X-linked juvenile retinoschisis (XLRS) is a hereditary retinal dystrophy in young males, caused by mutations in the RS1 gene. The function of the encoded protein, termed retinoschisin, and the molecular mechanisms underlying XLRS pathogenesis are still unresolved, although a direct interaction partner of the secreted retinoschisin, the retinal Na/K-ATPase, was recently identified. Earlier gene expression studies in retinoschisin-deficient (Rs1h

Indexed as

ApoptosisMAP Kinase Signaling SystemAnimalsCell Adhesion MoleculesExtracellular Signal-Regulated MAP KinasesExtracellular SpaceEye ProteinsGene Expression RegulationHEK293 CellsHumansMice, Inbred C57BLMutant ProteinsProtein BindingRetinaRetinoschisisCell Adhesion MoleculesExtracellular Signal-Regulated MAP KinasesEye ProteinsMutant ProteinsRS1 protein, mouseapoptosisMAP kinase signallingNa/K-ATPaseretinoschisinRS1X-linked juvenile retinoschisis

Identifiers

PMID27995734
PMCPMC5345684
OpenAlexW2562598511

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.