Evidence map›Paper›PMID 29880644›Full record

ArticleThe Journal of biological chemistry2018

LRRC8/VRAC anion channels are required for late stages of spermatid development in mice.

Jennifer C Lück, Dmytro Puchkov, Florian Ullrich, Thomas J Jentsch

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

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  14. Review
  15. Late adolescence mortality in mice with brain-specific deletion of the volume-regulated anion channel subunit LRRC8A.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
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  20. Observational
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.

Jennifer C LückFrom the Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), D-13125 Berlin, Germany.
Dmytro PuchkovFrom the Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), D-13125 Berlin, Germany.
Florian UllrichFrom the Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), D-13125 Berlin, Germany.ORCID 0000-0002-1153-2040
Thomas J JentschFrom the Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), D-13125 Berlin, Germany, Jentsch@fmp-berlin.de.ORCID 0000-0002-3509-2553

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spermatogenesis is a highly complex developmental process that occurs primarily in seminiferous tubules of the testes and requires additional maturation steps in the epididymis and beyond. Mutations in many different genes can lead to defective spermatozoa and hence to male infertility. Some of these genes encode for ion channels and transporters that play roles in various processes such as cellular ion homeostasis, signal transduction, sperm motility, and the acrosome reaction. Here we show that germ cell-specific, but not Sertoli cell-specific, disruption of

Indexed as

Gene DeletionSpermatogenesisAnimalsAnionsCell SizeInfertility, MaleIon ChannelsMaleMembrane ProteinsMiceMice, Inbred C57BLMitochondriaSpermatidsSpermatozoaSperm MotilityAnionsIon ChannelsLRRC8A protein, mouseMembrane ProteinsCl-channeleboICl, swellICl, volion channelmembrane proteinmitochondriamouseplasma membranespermatogenesisspermatozoaswelling-activated chloride channelVSOR

Identifiers

PMID29880644
PMCPMC6066314

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Registered trials

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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.