Evidence map›Paper›PMID 25567359›Full record

ArticleThe Journal of membrane biology2015

Effects on channel properties and induction of cell death induced by c-terminal truncations of pannexin1 depend on domain length.

Kathrin Engelhardt, Matthias Schmidt, Matthias Tenbusch, Rolf Dermietzel

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In one paragraph

Article in The Journal of membrane biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Pannexin1 as mediator of inflammation and cell death.Biochimica et biophysica acta. Molecular cell research · 2017
    Review
  7. Article
  8. Article
  9. 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 1 institution in 1 country.

Kathrin EngelhardtDepartment of Neuroanatomy and Molecular Brain Research, Ruhr-University Bochum, 44780, Bochum, Germany.
Matthias Schmidt
Matthias Tenbusch
Rolf Dermietzel
Ruhr University Bochum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pannexin1 (Panx1) is an integral membrane protein and known to form multifunctional hexameric channels. Recently, Panx1 was identified to be responsible for the release of ATP and UTP from apoptotic cells after site-specific proteolysis by caspases 3/7. Cleavage at the carboxy-terminal (CT) position aa 376-379 irreversibly opens human Panx1 channels and leads to the release of the respective nucleotides resulting in recruitment of macrophages and in subsequent activation of the immunologic response. The fact that cleavage of the CT at this particular residues terminates in a permanently open channel raised the issue of functional relevance of the CT of Panx1 for regulating channel properties. To analyze the impact of the CT on channel gating, we generated 14 truncated versions of rat Panx1 cleaved at different positions in the C-terminus. This allowed elaboration of the influence of defined residues on channel formation, voltage-dependent gating, execution of cell mortality, and susceptibility to the Panx1 inhibitor carbenoxolone. We demonstrate that expression of Panx1 proteins, which were truncated to lengths between 370 and 393 residues, induces differential effects after expression in Xenopus laevis oocytes as well as in Neuro2A cells with strongest impact downstream the caspase 3/7 cleavage site.

Indexed as

Protein Interaction Domains and MotifsAnimalsCell DeathCell LineCell SurvivalConnexinsGene ExpressionMembrane PotentialsNerve Tissue ProteinsOocytesRatsTransfectionXenopusConnexinsNerve Tissue Proteinspannexin 1, rat

Identifiers

PMID25567359
OpenAlexW1984239819

What OpenQuestion holds

Textmetadata
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.