Evidence map›Paper›PMID 16495337›Full record

ArticleMolecular biology of the cell2006

Caspase-2-induced apoptosis requires bid cleavage: a physiological role for bid in heat shock-induced death.

Christine Bonzon, Lisa Bouchier-Hayes, Lisa J Pagliari, Douglas R Green, Donald D Newmeyer

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 153 citations in OpenAlex.

  1. Article
  2. Article
  3. The efficacy of hyperthermia-based multimodal therapy is dependent on gatekeeper protein, BID.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
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  12. Review
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  14. Article
  15. Review
  16. Review
  17. Caspase-2 Substrates: To Apoptosis, Cell Cycle Control, and Beyond.Frontiers in cell and developmental biology · 2020
    Review
  18. Article
  19. Article
  20. Necroptosis andFrontiers in microbiology · 2019
    Article

18 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

5 authors at 1 institution in 1 country.

Christine BonzonDepartment of Molecular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA.
Lisa Bouchier-Hayes
Lisa J Pagliari
Douglas R Green
Donald D Newmeyer
La Jolla Institute for Immunology · US

Funding

THE ANTI-APOPTOTIC ROLE OF HEATSHOCK PROTEIN 70 (HSP 70)R01AI047891 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI GREEN, DOUGLAS R. · 2000 to 2014
$5.2M
MITOCHONDRIAL FUNCTION IN APOPTOSISR01GM062289 · NIGMS · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI NEWMEYER, DONALD DAVID · 2001 to 2013
$4.3M
Mitochondrial Pathways in ApoptosisR01GM050284 · NIGMS · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI NEWMEYER, DONALD DAVID · 1997 to 2009
$2.8M
NIAID NIH HHS AI47891NIAID NIH HHS R01 AI047891NIGMS NIH HHS GM50284NIGMS NIH HHS GM62289NIGMS NIH HHS R01 GM050284NIGMS NIH HHS R01 GM062289
6 · The paper itself

Abstract

The mechanisms through which Caspase-2 leads to cell death are controversial. Here we show, using a combination of cell-free and cell culture-based approaches, that cleavage of the Bcl-2-family protein Bid is required for the induction of apoptosis by Caspase-2. Caspase-2 promoted cytochrome c release from mitochondria in the presence of cytosol from wild-type, but not Bid-deficient, mouse embryonic fibroblasts (MEFs). Recombinant wild-type Bid, but not a noncleavable mutant (D59E), restored cytochrome c release. Similarly, Bid-null MEFs were relatively resistant to apoptosis triggered by active Caspase-2, and apoptosis was restored in Bid-null cells by the expression of wild-type, but not D59E, Bid. Finally, Bid-null MEFs were substantially more resistant to apoptosis induced by heat shock, which has been shown to be dependent on apical activation of Caspase-2. The data are consistent with a model in which Caspase-2 induces apoptosis via cleavage of Bid at D59 and the subsequent engagement of the mitochondrial (intrinsic) pathway.

Indexed as

ApoptosisHot TemperatureAnimalsBH3 Interacting Domain Death Agonist ProteinCaspase 2CaspasesCells, CulturedCytochromes cCytosolEmbryo, MammalianEnzyme ActivationFibroblastsMiceMitochondriaMutationBH3 Interacting Domain Death Agonist ProteinBid protein, mouseCaspase 2CaspasesCytochromes c

Identifiers

PMID16495337
PMCPMC1446087
OpenAlexW2132106223

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.