Evidence map›Paper›PMID 23539542›Full record

ArticleJournal of clinical & cellular immunology2012

Promotion of Caspase Activation by Caspase-9-mediated Feedback Amplification of Mitochondrial Damage.

Alan D Guerrero, Ingo Schmitz, Min Chen, Jin Wang

Abstract read
In one paragraph

Article in Journal of clinical & cellular immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Role of BRCA1 in glioblastoma etiology.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
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  8. Revisiting Regulated Cell Death Responses in Viral Infections.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Induction of apoptosis by total flavonoids from Scutellaria barbata D. Don in human hepatocarcinoma MHCC97-H cells via the mitochondrial pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  19. 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.

Alan D GuerreroDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, Texas 77030, USA.
Ingo Schmitz
Min Chen
Jin Wang
Baylor College of Medicine · US

Funding

Roles of Dendritic Cells in Immune RegulationR01AI074949 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI WANG, JIN · 2007 to 2011
$1.7M
Molecular Regulation of Erythroid DifferentiationR01DK083164 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHEN, MIN · 2009 to 2013
$1.5M
Activation and in vivo Functions of Initiator CaspasesR01GM087710 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI WANG, JIN · 2009 to 2012
$1.4M
NIAID NIH HHS R01 AI074949NIDDK NIH HHS R01 DK083164NIGMS NIH HHS R01 GM087710
6 · The paper itself

Abstract

Mitochondrial disruption during apoptosis results in the activation of caspase-9 and a downstream caspase cascade. Triggering this caspase cascade leads to the cleavage of anti-apoptotic Bcl-2 family proteins, resulting in feedback amplification of mitochondrial disruption. However, whether such a feedback loop plays an important role in the promotion of caspase activation and execution of apoptosis has not been well established. We observed that mutated Bcl-2 or Bcl-xL that are resistant to cleavage by caspases inhibited caspase-9-induced caspase activation in human H9 T cells. The release of Smac after the activation of caspase-9 was also inhibited by cleavage-resistant Bcl-2 or Bcl-xL. Consistently, caspase-9-deficient cells were defective in the release of Smac after induction of apoptosis. Moreover, addition of a Smac mimetic overcame the inhibitory effects of cleavage-resistant Bcl-2/Bcl-xL, and restored caspase-9-mediated cell death. Our data suggest that caspase-9-induced feedback disruption of mitochondria plays an important role in promoting the activation of caspases, while a defect in this process can be overcome by promoting Smac functions.

Indexed as

bcl-2bcl-xLcaspase-9mitochondrial feedback

Identifiers

PMID23539542
PMCPMC3607397
OpenAlexW2151419515

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.