ArticleOncogene2008
Bfl-1/A1 functions, similar to Mcl-1, as a selective tBid and Bak antagonist.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 73 citations in OpenAlex.
- Postnatal Exposure Sensitizes for Zinc/Paraquat-Induced Neuronal Apoptosis, Adulthood Exposure Leads to the Final Effects.Journal of molecular neuroscience : MN · 2026Article
- Bcl-2 modifying factor (Bmf): "a mysterious stranger" in the Bcl-2 family proteins.Cell death and differentiation · 2026Review
- Deciphering molecular specificity in MCL-1/BAK interaction and its implications for designing potent MCL-1 inhibitors.Cell death and differentiation · 2025Article
- MCL‑1 safeguards activated hair follicle stem cells to enable adult hair regeneration.Nature communications · 2025Article
- Molecular Cell Biology of Apoptosis in Health and Disease.Advances in experimental medicine and biology · 2025Review
- Identification and Evaluation of Reversible Covalent Binders to Cys55 of Bfl-1 from a DNA-Encoded Chemical Library Screen.ACS medicinal chemistry letters · 2024Article
- Directly targeting BAX for drug discovery: Therapeutic opportunities and challenges.Acta pharmaceutica Sinica. B · 2024Review
- Mechanisms of BCL-2 family proteins in mitochondrial apoptosis.Nature reviews. Molecular cell biology · 2023Review
- Last but not least: BFL-1 as an emerging target for anti-cancer therapies.Biochemical Society transactions · 2022Review
- Article
- The Stress-Inducible BCL2A1 Is Required for Ovarian Cancer Metastatic Progression in the Peritoneal Microenvironment.Cancers · 2021Article
- NF-κB activity during pancreas development regulates adult β-cell mass by modulating neonatal β-cell proliferation and apoptosis.Cell death discovery · 2021Article
- Physiological Functions of Mcl-1: Insights From Genetic Mouse Models.Frontiers in cell and developmental biology · 2021Review
- Article
- Discovery and Characterization of 2,5-Substituted Benzoic Acid Dual Inhibitors of the Anti-apoptotic Mcl-1 and Bfl-1 Proteins.Journal of medicinal chemistry · 2020Article
- Infection with flaviviruses requires BCLXL for cell survival.PLoS pathogens · 2018Article
- Angiotensin II type 2 receptor promotes apoptosis and inhibits angiogenesis in bladder cancer.Journal of experimental & clinical cancer research : CR · 2017Article
- Constitutive expression of the anti-apoptotic Bcl-2 family member A1 in murine endothelial cells leads to transplant tolerance.Clinical and experimental immunology · 2017Article
- Article
- Francisella tularensis Modulates a Distinct Subset of Regulatory Factors and Sustains Mitochondrial Integrity to Impair Human Neutrophil Apoptosis.Journal of innate immunity · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The prosurvival Bcl-2-family member Bfl-1/A1 is a transcriptional target of nuclear factor-kappaB (NF-kappaB) that is overexpressed in many human tumors and is a means by which NF-kappaB inhibits apoptosis, but its mode of action is controversial. To better understand how Bfl-1 functions, we investigated its interaction with proapoptotic multidomain proteins Bax and Bak, and the BH3-only proteins Bid and tBid. We demonstrate that in living cells Bfl-1 selectively interacts with Bak and tBid, but not with Bax or Bid. Bfl-1/Bak interaction is functional as Bfl-1 suppressed staurosporine (STS)-induced apoptosis in wild-type and Bax-deficient cells, but not in Bak-/- cells. We also show that Bfl-1 blocks tumor necrosis factor-alpha (TNFalpha)-induced activation of Bax indirectly, via association with tBid. C-terminal deletion decreased Bfl-1's interaction with Bak and tBid and reduced its ability to suppress Bak- and tBid-mediated cell death. These data indicate that Bfl-1 utilizes different mechanisms to suppress apoptosis depending on the stimulus. Bfl-1 associates with tBid to prevent activation of proapoptotic Bax and Bak, and it also interacts directly with Bak to antagonize Bak-mediated cell death, similar to Mcl-1. Thus, part of the protective function of NF-kappaB is to induce Mcl-1-like activity by upregulating Bfl-1.
Indexed as
Identifiers
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.