Evidence map›Paper›PMID 28124625›Full record

ReviewBMC cell biology2017

Gap junctions and hemichannels: communicating cell death in neurodevelopment and disease.

Andrei B Belousov, Joseph D Fontes, Moises Freitas-Andrade, Christian C Naus

Open access · goldAbstract readReview
In one paragraph

Review in BMC cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
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  7. Article
  8. Role of astrocytes connexins - pannexins in acute brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  9. Ginsenoside RbChinese herbal medicines · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Purinergic Signalling in the Cochlea.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Review
  19. Review
  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

4 authors at 2 institutions in 2 countries.

Andrei B BelousovDepartment of Molecular & Integrative Physiology, University of Kansas Medical Center, The University of Kansas, Kansas City, KS, 66160, USA.
Joseph D FontesDepartment of Biochemistry and Molecular Biology, University of Kansas Medical Center, The University of Kansas, Kansas City, KS, 66160, USA.
Moises Freitas-AndradeDepartment of Cellular & Physiological Sciences, Faculty of Medicine, Life Sciences Institute, The University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada.
Christian C NausDepartment of Cellular & Physiological Sciences, Faculty of Medicine, Life Sciences Institute, The University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada. christian.naus@ubc.ca.
University of British Columbia · CAUniversity of Kansas Medical Center · US

Funding

NOVEL MECHANISM FOR GLUTAMATE-DEPENDENT EXCITOTOXICITYR21NS076925 · NINDS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BELOUSOV, ANDREI B · 2012 to 2013
$409k
CIHRNINDS NIH HHS R21 NS076925
6 · The paper itself

Abstract

Gap junctions are unique membrane channels that play a significant role in intercellular communication in the developing and mature central nervous system (CNS). These channels are composed of connexin proteins that oligomerize into hexamers to form connexons or hemichannels. Many different connexins are expressed in the CNS, with some specificity with regard to the cell types in which distinct connexins are found, as well as the timepoints when they are expressed in the developing and mature CNS. Both the main neuronal Cx36 and glial Cx43 play critical roles in neurodevelopment. These connexins also mediate distinct aspects of the CNS response to pathological conditions. An imbalance in the expression, translation, trafficking and turnover of connexins, as well as mutations of connexins, can impact their function in the context of cell death in neurodevelopment and disease. With the ever-increasing understanding of connexins in the brain, therapeutic strategies could be developed to target these membrane channels in various neurological disorders.

Indexed as

Cell CommunicationAnimalsCell DeathConnexinsGap JunctionsHumansNervous SystemNervous System DiseasesConnexins

Identifiers

PMID28124625
PMCPMC5267333
OpenAlexW2578846619

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.