Evidence map›Paper›PMID 34073084›Full record

ReviewLife (Basel, Switzerland)2021

The ATP-Releasing Maxi-Cl Channel: Its Identity, Molecular Partners and Physiological/Pathophysiological Implications.

Ravshan Z Sabirov, Md Rafiqul Islam, Toshiaki Okada, Petr G Merzlyak, Ranokhon S Kurbannazarova, Nargiza A Tsiferova, Yasunobu Okada

Open access · goldAbstract readReview
In one paragraph

Review in Life (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
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  4. Pathogenesis of chronic enteropathy associated with theWorld journal of gastroenterology · 2024
    Review
  5. ATP functions as a primary alarmin in allergen-induced type 2 immunity.American journal of physiology. Cell physiology · 2023
    Review
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  7. Review
  8. Review
  9. Article
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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

7 authors at 3 institutions in 3 countries.

Ravshan Z SabirovDivision of Cell Signaling, National Institute for Physiological Sciences (NIPS), Okazaki 444-8787, Japan.
Md Rafiqul IslamDivision of Cell Signaling, National Institute for Physiological Sciences (NIPS), Okazaki 444-8787, Japan.
Toshiaki OkadaDivision of Cell Signaling, National Institute for Physiological Sciences (NIPS), Okazaki 444-8787, Japan.
Petr G MerzlyakDivision of Cell Signaling, National Institute for Physiological Sciences (NIPS), Okazaki 444-8787, Japan.ORCID 0000-0002-7733-7598
Ranokhon S KurbannazarovaDivision of Cell Signaling, National Institute for Physiological Sciences (NIPS), Okazaki 444-8787, Japan.
Nargiza A TsiferovaDivision of Cell Signaling, National Institute for Physiological Sciences (NIPS), Okazaki 444-8787, Japan.
Yasunobu OkadaDivision of Cell Signaling, National Institute for Physiological Sciences (NIPS), Okazaki 444-8787, Japan.
National Institute for Physiological Sciences · JPAichi Medical University · JPJagannath University · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Maxi-Cl phenotype accounts for the majority (app. 60%) of reports on the large-conductance maxi-anion channels (MACs) and has been detected in almost every type of cell, including placenta, endothelium, lymphocyte, cardiac myocyte, neuron, and glial cells, and in cells originating from humans to frogs. A unitary conductance of 300-400 pS, linear current-to-voltage relationship, relatively high anion-to-cation selectivity, bell-shaped voltage dependency, and sensitivity to extracellular gadolinium are biophysical and pharmacological hallmarks of the Maxi-Cl channel. Its identification as a complex with SLCO2A1 as a core pore-forming component and two auxiliary regulatory proteins, annexin A2 and S100A10 (p11), explains the activation mechanism as Tyr23 dephosphorylation at ANXA2 in parallel with calcium binding at S100A10. In the resting state, SLCO2A1 functions as a prostaglandin transporter whereas upon activation it turns to an anion channel. As an efficient pathway for chloride, Maxi-Cl is implicated in a number of physiologically and pathophysiologically important processes, such as cell volume regulation, fluid secretion, apoptosis, and charge transfer. Maxi-Cl is permeable for ATP and other small signaling molecules serving as an electrogenic pathway in cell-to-cell signal transduction. Mutations at the

Indexed as

ANXA2ATP releasebiophysical propertiesdiseasesglutamate releasemaxi-anion channelsMaxi-Clpurinergic signalingS100A10SLCO2A1

Identifiers

PMID34073084
PMCPMC8229958
OpenAlexW3164592152

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.