Evidence map›Paper›PMID 25779082›Full record

ArticleBiochimica et biophysica acta2015

Role of Akt and Ca2+ on cell permeabilization via connexin43 hemichannels induced by metabolic inhibition.

Daniela Salas, Carlos Puebla, Paul D Lampe, Sergio Lavandero, Juan C Sáez

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Acute activation of hemichannels by ethanol leads to CaFrontiers in cell and developmental biology · 2024
    Article
  4. Review
  5. Protein kinase B (AKT) upregulation and Thy-1-αJournal of neuroinflammation · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. 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

5 authors at 4 institutions in 2 countries.

Daniela SalasAdvanced Center for Chronic Diseases (ACCDIS) & Centro Estudios Moleculares de la Célula (CMEC), Facultad Ciencias Químicas y Farmacéuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile; Departamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile. Electronic address: danielasalas@gmail.com.
Carlos PueblaDepartamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile.
Paul D LampeTranslational Research Program, Human Biology and Public Health Sciences Divisions, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.
Sergio LavanderoAdvanced Center for Chronic Diseases (ACCDIS) & Centro Estudios Moleculares de la Célula (CMEC), Facultad Ciencias Químicas y Farmacéuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile.
Juan C SáezDepartamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile; Instituto Milenio, Centro Interdisciplinario de Neurociencias de Valparaíso, Valparaíso, Chile. Electronic address: jsaez@bio.puc.cl.
Pontificia Universidad Católica de Chile · CLAdvanced Center for Chronic Diseases · CLFred Hutch Cancer Center · USValparaiso University · US

Funding

PHOSPHORYLATION OF GAP JUNCTION PROTEINSR01GM055632 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI LAMPE, PAUL D. · 1997 to 2017
$6.1M
NIGMS NIH HHS GM55632NIGMS NIH HHS R01 GM055632
6 · The paper itself

Abstract

Connexin hemichannels are regulated under physiological and pathological conditions. Metabolic inhibition, a model of ischemia, promotes surface hemichannel activation associated, in part, with increased surface hemichannel levels, but little is known about its underlying mechanism. Here, we investigated the role of Akt on the connexin43 hemichannel's response induced by metabolic inhibition. In HeLa cells stably transfected with rat connexin43 fused to EGFP (HeLa43 cells), metabolic inhibition induced a transient Akt activation necessary to increase the amount of surface connexin43. The increase in levels of surface connexin43 was also found to depend on an intracellular Ca2+ signal increase that was partially mediated by Akt activation. However, the metabolic inhibition-induced Akt activation was not significantly affected by intracellular Ca2+ chelation. The Akt-dependent increase in connexin43 hemichannel activity in HeLa43 cells also occurred after oxygen-glucose deprivation, another ischemia-like condition, and in cultured cortical astrocytes (endogenous connexin43 expression system) under metabolic inhibition. Since opening of hemichannels has been shown to accelerate cell death, inhibition of Akt-dependent phosphorylation of connexin43 hemichannels could reduce cell death induced by ischemia/reperfusion.

Indexed as

AnimalsApoptosisAstrocytesCalciumCell HypoxiaCell Membrane PermeabilityCells, CulturedConnexin 43GlucoseHeLa CellsHumansProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyCalciumConnexin 43GlucoseProto-Oncogene Proteins c-aktAkt activationIntracellular Ca(2+)Oxygen-glucose deprivationSurface hemichannels

Identifiers

PMID25779082
PMCPMC4476395
OpenAlexW2080018885

What OpenQuestion holds

Textmetadata
LicenceTDM
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.