ReviewTrends in biochemical sciences2014
Many players in BCL-2 family affairs.
Review in Trends in biochemical sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers.
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.
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.
Who cites it
196 citing papers in PubMed.
- Investigating the role of Zibai ointment on apoptosis-related factors Bcl-2 and Bax in wound healing after anal fistula surgery.Immunity, inflammation and disease · 2023Trial
- MAP30, a type Ⅰ ribosome-inactivating protein, inhibits hepatocellular carcinoma by inducing apoptosis through mitochondria.Medicine · 2026Article
- A century of cell death research.Journal of cell science · 2026Review
- BAX as a Biomarker for Predicting Immunotherapeutic Efficacy in Uveal Melanoma Patients: A Comprehensive Analysis.Molecular biotechnology · 2026Article
- DrugBank mining with machine learning reveals novel candidates for BCL-2 inhibition.Scientific reports · 2026Article
- Revealing the landscape of targeting mitochondrial functions and behaviors to overcome cancer chemoresistance.Journal of the National Cancer Center · 2025Review
- Molecular mechanisms underlying HRK interaction with BCL-XL and BCL-2 reveal specificity determinants for BH3 mimetics.iScience · 2025Article
- Deciphering molecular specificity in MCL-1/BAK interaction and its implications for designing potent MCL-1 inhibitors.Cell death and differentiation · 2025Article
- Collaborative orchestration of BH3-only proteins governs Bak/Bax-dependent hepatocyte apoptosis under antiapoptotic protein-deficiency in mice.Cell death and differentiation · 2025Article
- Histological, immunohistochemical assessment and DNA fingerprint species identification of some meat products in Egypt.Scientific reports · 2025Article
- Structural basis of BAK sequestration by MCL-1 in apoptosis.Molecular cell · 2025Article
- MCL‑1 safeguards activated hair follicle stem cells to enable adult hair regeneration.Nature communications · 2025Article
- Carbon ion irradiation conquers the radioresistance by inducing complex DNA damage and apoptosis in U251 human glioblastomas cells.Medical oncology (Northwood, London, England) · 2025Article
- Emerging opportunities to treat drug-resistant breast cancer: Discovery of novel small-molecule inhibitors against different targets.Frontiers in pharmacology · 2025Review
- Review
- An Azomethine Derivative, BCS3, Targets XIAP and cIAP1/2 to Arrest Breast Cancer Progression Through MDM2-p53 and Bcl-2-Caspase Signaling Modulation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- BET inhibitors (BETi) influence oxidative phosphorylation metabolism by affecting mitochondrial dynamics leading to alterations in apoptotic pathways in triple-negative breast cancer (TNBC) cells.Cell proliferation · 2024Article
- Gene Expression Regulation and the Signal Transduction of Programmed Cell Death.Current issues in molecular biology · 2024Review
- BCL-2 inhibitors in hematological malignancies: biomarkers that predict response and management strategies.Frontiers in oncology · 2024Review
- Article
136 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
During apoptotic cell death, cellular stress signals converge at the mitochondria to induce mitochondrial outer-membrane permeabilization (MOMP) through B cell lymphoma-2 (BCL-2) family proteins and their effectors. BCL-2 proteins function through protein-protein interactions, the mechanisms and structural aspects of which are only now being uncovered. Recently, the elucidation of the dynamic features underlying their function has highlighted their structural plasticity and the consequent complex thermodynamic landscape governing their protein-protein interactions. These studies show that canonical interactions involve a conserved, hydrophobic groove, whereas non-canonical interactions function allosterically outside the groove. We review the latest structural advances in understanding the interactions and functions of mammalian BCL-2 family members, and discuss new opportunities to modulate these proteins in health and disease.
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What OpenQuestion holds
Registered trials
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.