Evidence map›Paper›PMID 21720385›Full record

ArticleCell death and differentiation2012

VDAC1 selectively transfers apoptotic Ca2+ signals to mitochondria.

D De Stefani, A Bononi, A Romagnoli, A Messina, V De Pinto, P Pinton, R Rizzuto

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

173 citing papers in PubMed, 305 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Migrasomes in Ischemic Stroke: Molecular Landscape and Pathophysiological Impact.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

113 more citing papers are in PubMed but not listed here.

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 1 country.

D De StefaniDepartment of Biomedical Sciences, University of Padova and CNR Neuroscience Institute, Padua, Italy.
A Bononi
A Romagnoli
A Messina
V De Pinto
P Pinton
R Rizzuto
Neuroscience Institute · ITUniversity of Catania · ITUniversity of Ferrara · IT

Funding

TRANSLOCATION OF p66Shc: KINETICS, FUNCTION, APOPTOSISP01AG025532 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KIM, KYOUNGMI · 2007 to 2017
$12.1M
NIA NIH HHS 1P01AG025532-01A1NIA NIH HHS P01 AG025532Telethon GGP11082Telethon GGP11139Telethon GPP10005
6 · The paper itself

Abstract

Voltage-dependent anion channels (VDACs) are expressed in three isoforms, with common channeling properties and different roles in cell survival. We show that VDAC1 silencing potentiates apoptotic challenges, whereas VDAC2 has the opposite effect. Although all three VDAC isoforms are equivalent in allowing mitochondrial Ca(2+) loading upon agonist stimulation, VDAC1 silencing selectively impairs the transfer of the low-amplitude apoptotic Ca(2+) signals. Co-immunoprecipitation experiments show that VDAC1, but not VDAC2 and VDAC3, forms complexes with IP(3) receptors, an interaction that is further strengthened by apoptotic stimuli. These data highlight a non-redundant molecular route for transferring Ca(2+) signals to mitochondria in apoptosis.

Indexed as

ApoptosisCalcium SignalingCalciumGene SilencingHeLa CellsHumansHydrogen PeroxideImmunoprecipitationInositol 1,4,5-Trisphosphate ReceptorsMitochondriaProtein IsoformsVoltage-Dependent Anion Channel 1CalciumHydrogen PeroxideInositol 1,4,5-Trisphosphate ReceptorsProtein IsoformsVoltage-Dependent Anion Channel 1

Identifiers

PMID21720385
PMCPMC3263501
OpenAlexW1999030622

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.