Evidence map›Paper›PMID 22978471›Full record

ReviewAntioxidants & redox signaling2013

Regulation of the intrinsic apoptosis pathway by reactive oxygen species.

Chu-Chiao Wu, Shawn B Bratton

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

216 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Investigating Vitamin DMolecular diversity · 2026
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

156 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

2 authors.

Chu-Chiao WuInstitute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas, USA.
Shawn B Bratton

Funding

Heat shock-induced apoptosisR01CA129521 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BRATTON, SHAWN B · 2008 to 2012
$1.5M
Caspase-activating ComplexesR01GM096101 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BRATTON, SHAWN B · 2011 to 2014
$1.2M
NCI NIH HHS R01CA129521NIGMS NIH HHS R01 GM096101NIGMS NIH HHS R01GM096101
6 · The paper itself

Abstract

significanceThe intrinsic apoptosis pathway is conserved from worms to humans and plays a critical role in the normal development and homeostatic control of adult tissues. As a result, numerous diseases from cancer to neurodegeneration are associated with either too little or too much apoptosis. RECENT ADVANCES: B cell lymphoma-2 (BCL-2) family members regulate cell death, primarily via their effects on mitochondria. In stressed cells, proapoptotic BCL-2 family members promote mitochondrial outer membrane permeabilization (MOMP) and cytochrome c (cyt c) release into the cytoplasm, where it stimulates formation of the "apoptosome." This large, multimeric complex is composed of the adapter protein, apoptotic protease-activating factor-1, and the cysteine protease, caspase-9. Recent studies suggest that proteins involved in the processes leading up to (and including) formation of the apoptosome are subject to various forms of post-translational modification, including proteolysis, phosphorylation, and in some cases, direct oxidative modification. CRITICAL ISSUES: Despite intense investigation of the intrinsic pathway, significant questions remain regarding how cyt c is released from mitochondria, how the apoptosome is formed and regulated, and how caspase-9 is activated within the complex. FUTURE DIRECTIONS: Further studies on the biochemistry of MOMP and apoptosome formation are needed to understand the mechanisms that underpin these critical processes, and novel animal models will be necessary in the future to ascertain the importance of the many posttranslational modifications reported for BCL-2 family members and components of the apoptosome.

Indexed as

ApoptosisAnimalsCaspase 9Cytochromes cHumansMitochondrial MembranesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreOxidative StressPermeabilityProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesCASP9 protein, humanCaspase 9Cytochromes cMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreProto-Oncogene Proteins c-bcl-2Reactive Oxygen Species

Identifiers

PMID22978471
PMCPMC3717204

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.