Evidence map›Paper›PMID 33187987›Full record

ArticleThe Journal of biological chemistry

Cellular basis of ClC-2 Cl

Corinna Göppner, Audrey H Soria, Maja B Hoegg-Beiler, Thomas J Jentsch

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Identification of a novelFrontiers in genetics · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Development of perivascular astrocyte processes.Frontiers in neuroscience · 2025
    Review
  9. Review
  10. Expanding the phenotypic spectrum ofBrain communications · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Chloride transport modulators as drug candidates.American journal of physiology. Cell physiology · 2021
    Review
  17. Apical CLC-2 in retinal pigment epithelium is crucial for survival of the outer retina.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  18. Article
  19. Review
  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

4 authors at 1 institution in 1 country.

Corinna GöppnerLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany; Max-Delbrück-Centrum für Molekulare Medizin (MDC), Berlin, Germany.
Audrey H SoriaLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany; Max-Delbrück-Centrum für Molekulare Medizin (MDC), Berlin, Germany.
Maja B Hoegg-BeilerLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany; Max-Delbrück-Centrum für Molekulare Medizin (MDC), Berlin, Germany.
Thomas J JentschLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany; Max-Delbrück-Centrum für Molekulare Medizin (MDC), Berlin, Germany; NeuroCure Cluster of Excellence, Charité Universitätsmedizin, Berlin, Germany. Electronic address: Jentsch@fmp-berlin.de.
Max Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ClC-2 chloride channel is expressed in the plasma membrane of almost all mammalian cells. Mutations that cause the loss of ClC-2 function lead to retinal and testicular degeneration and leukodystrophy, whereas gain-of-function mutations cause hyperaldosteronism. Leukodystrophy is also observed with a loss of GlialCAM, a cell adhesion molecule that binds to ClC-2 in glia. GlialCAM changes the localization of ClC-2 and opens the channel by altering its gating. We now used cell type-specific deletion of ClC-2 in mice to show that retinal and testicular degeneration depend on a loss of ClC-2 in retinal pigment epithelial cells and Sertoli cells, respectively, whereas leukodystrophy was fully developed only when ClC-2 was disrupted in both astrocytes and oligodendrocytes. The leukodystrophy of Glialcam

Indexed as

AnimalsAstrocytesBrain DiseasesCell Adhesion Molecules, Neuron-GliaCell Cycle ProteinsChloride ChannelsCLC-2 Chloride ChannelsHomeostasisHumansIon Channel GatingIronMaleMiceMice, KnockoutNerve Tissue ProteinsOligodendrogliaCell Adhesion Molecules, Neuron-GliaCell Cycle ProteinsChloride ChannelsCLC-2 Chloride ChannelsClcn2 protein, mouseGlialCAM protein, mouseHEPACAM protein, humanIronNerve Tissue Proteinsaldosteronismanion channelHepaCAMinfertilityleukoencephalopathymyelin vacuolizationRPE

Identifiers

PMID33187987
PMCPMC7949093
OpenAlexW3099401706

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.