Evidence map›Paper›PMID 26470731›Full record

ArticleCell death and differentiation2016

BAX inhibitor-1 is a Ca(2+) channel critically important for immune cell function and survival.

D Lisak, T Schacht, A Gawlitza, P Albrecht, O Aktas, B Koop, M Gliem, H H Hofstetter, K Zanger, G Bultynck and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. 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
1.5field-weighted citation impact, top 17% 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, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. [Bax inhibitor-1 inhibits calcification of vascular smooth muscle cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. iCaFrontiers in immunology · 2020
    Article
  10. Article
  11. Ion and pH Sensitivity of a TMBIM CaStructure (London, England : 1993) · 2019
    Article
  12. Article
  13. Review
  14. PeerJ · 2017
    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

19 authors at 7 institutions in 4 countries.

D LisakFocus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn) and Department of Neurology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
T SchachtFocus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn) and Department of Neurology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
A GawlitzaFocus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn) and Department of Neurology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
P AlbrechtHeinrich Heine Universität Düsseldorf, Department of Neurology, Düsseldorf, Germany.
O AktasHeinrich Heine Universität Düsseldorf, Department of Neurology, Düsseldorf, Germany.
B KoopHeinrich Heine Universität Düsseldorf, Department of Neurology, Düsseldorf, Germany.
M GliemHeinrich Heine Universität Düsseldorf, Department of Neurology, Düsseldorf, Germany.
H H HofstetterHeinrich Heine Universität Düsseldorf, Department of Neurology, Düsseldorf, Germany.
K ZangerCenter for Anatomy and Brain Research, Düsseldorf, Germany.
G BultynckLaboratory of Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine, KU Leuven, Belgium.
J B ParysLaboratory of Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine, KU Leuven, Belgium.
H De SmedtLaboratory of Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine, KU Leuven, Belgium.
T KindlerIII Medical Clinic, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
P Adams-QuackInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
M HahnInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
A WaismanInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
J C ReedSanford Burnham Institute, La Jolla, CA, USA.
N HövelmeyerInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
A MethnerFocus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn) and Department of Neurology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
University Medical Center of the Johannes Gutenberg University Mainz · DEHeinrich Heine University Düsseldorf · DEJohannes Gutenberg University Mainz · DEToxicologie, Pharmacologie et Signalisation Cellulaire · FRBrain (Germany) · DESanford Burnham Prebys Medical Discovery Institute · USVIB-KU Leuven Center for Cancer Biology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endoplasmic reticulum (ER) serves as the major intracellular Ca(2+) store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca(2+) leak channel also implicated in the response against protein misfolding, thereby connecting the Ca(2+) store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-κB (nuclear factor-κ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca(2+) levels. When put into culture, purified knockout T cells and even more so B cells die spontaneously. This is preceded by increased activity of the mitochondrial initiator caspase-9 and correlated with a significant surge in mitochondrial Ca(2+) levels, suggesting an exhausted mitochondrial Ca(2+) buffer capacity as the underlying cause for cell death in vitro. In vivo, T-cell-dependent experimental autoimmune encephalomyelitis and B-cell-dependent antibody production are attenuated, corroborating the ex vivo results. These results suggest that BI-1 has a major role in the functioning of the adaptive immune system by regulating intracellular Ca(2+) homeostasis in lymphocytes.

Indexed as

Active Transport, Cell NucleusAnimalsApoptosisB-LymphocytesCalciumCalcium SignalingCaspasesCell SurvivalCytoplasmEncephalomyelitis, Autoimmune, ExperimentalEndoplasmic ReticulumEnzyme ActivationFemaleLeukopeniaMembrane ProteinsMice, Inbred C57BLCalciumCaspasesMembrane ProteinsNF-kappa BTmbim6 protein, mouse

Identifiers

PMID26470731
PMCPMC4716298
OpenAlexW2408541095

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.