Evidence map›Paper›PMID 19641503›Full record

ReviewOncogene2008

BH3-only proteins in apoptosis and beyond: an overview.

E Lomonosova, G Chinnadurai

Open access · greenAbstract readComparative StudyReview
In one paragraph

Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

242 citing papers in PubMed, 434 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Upregulation of a CircularInternational journal of molecular sciences · 2026
    Article
  5. Article
  6. Article
  7. High uPAR and Low miR-221 Expression Predict Poor Disease-Free Survival in Triple-Negative Breast Cancer.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Predicting Protein Cascade Expression from H&E Images.medRxiv : the preprint server for health sciences · 2026
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Advances inMicroorganisms · 2025
    Review
  19. Article
  20. Crack Cocaine Smoke Induces Tissue Degeneration in Rat Submandibular Glands by Toll-like Signaling Pathway.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article

182 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 at 1 institution in 1 country.

E LomonosovaInstitute for Molecular Virology, Saint Louis University School of Medicine, Doisy Research Center, St Louis, MO 63104, USA.
G Chinnadurai
Saint Louis University · US

Funding

PROMOTION OF CELL SURVIVAL BY ADENOVIRUS E1B 19K PROTEINR01CA033616 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 1985 to 2015
$4.0M
ONCOGENIC AND CHEMORESISTANCE BY BCL 2R01CA073803 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 1998 to 2008
$2.0M
BH3-only protein BNIP3 in tumor progressionR21CA116262 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 2005 to 2006
$250k
NCI NIH HHS CA-116262NCI NIH HHS CA-33616NCI NIH HHS CA-73803NCI NIH HHS R01 CA033616NCI NIH HHS R01 CA073803NCI NIH HHS R21 CA116262
6 · The paper itself

Abstract

BH3-only BCL-2 family proteins are effectors of canonical mitochondrial apoptosis. They discharge their pro-apoptotic functions through BH1-3 pro-apoptotic proteins such as BAX and BAK, while their activity is suppressed by BH1-4 anti-apoptotic BCL-2 family members. The precise mechanism by which BH3-only proteins mediate apoptosis remains unresolved. The existing data are consistent with three mutually non-exclusive models (1) displacement of BH1-3 proteins from complexes with BH1-4 proteins; (2) direct interaction with and conformational activation of BH1-3 proteins; and (3) membrane insertion and membrane remodeling. The BH3-only proteins appear to play critical roles in restraining cancer and inflammatory diseases such as rheumatoid arthritis. Molecules that mimic the effect of BH3-only proteins are being used in treatments against these diseases. The cell death activity of a subclass of BH3-only members (BNIP3 and BNIP3L) is linked to cardiomyocyte loss during heart failure. In addition to their established role in apoptosis, several BH3-only members also regulate diverse cellular functions in cell-cycle regulation, DNA repair and metabolism. Several members are implicated in the induction of autophagy and autophagic cell death, possibly through unleashing of the BH3-only autophagic effector Beclin 1 from complexes with BCL-2/BCL-xL. The Chapters included in the current Oncogene Review issues provide in-depth discussions on various aspects of major BH3-only proteins.

Indexed as

Amino Acid SequenceAnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsArthritis, RheumatoidAutophagyCaenorhabditis elegans ProteinsCell CycleCell Transformation, NeoplasticConsensus SequenceGene Expression RegulationHeart FailureHumansMammalsMiceAntineoplastic AgentsApoptosis Regulatory ProteinsBax protein (53-86)Caenorhabditis elegans ProteinsPeptide FragmentsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID19641503
PMCPMC2928556
OpenAlexW1999653222

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.