ArticleCancer cell2017
Direct Activation of BAX by BTSA1 Overcomes Apoptosis Resistance in Acute Myeloid Leukemia.
Article in Cancer cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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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.
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Who cites it
87 citing papers in PubMed, 159 citations in OpenAlex.
- DecipheringGenes · 2026Article
- 2-Pyrazoline-5-One Derivative Suppresses Cell Proliferation and Induces Apoptosis With Upregulation of Bax in Breast Cancer Cells.Journal of biochemical and molecular toxicology · 2026Article
- Article
- Ubiquitin-Specific Protease 49 Interacts with Bax to Modulate Apoptosis.International journal of molecular sciences · 2026Article
- A smart gene circuit for precise regulation of tumor cell behavior.Synthetic and systems biotechnology · 2026Article
- A gated hydrophobic funnel within BAX binds bioactive lipids to potentiate pro-apoptotic function.Nature communications · 2026Article
- Article
- Lapatinib Promotes Apoptosis in Hepatoma Cells by Regulating SPP1 Expression.Anti-cancer agents in medicinal chemistry · 2026Article
- Targeting cell death pathways in acute myeloid leukemia: Molecular mechanisms and clinical implications (Review).Oncology reports · 2025Review
- Activatable companion theranostics for dual-modality imaging-escorted pyroptosis-propelled synergistic cancer therapy.Bioactive materials · 2025Article
- Phytochemical Characterization and Anticancer Activity ofInternational journal of molecular sciences · 2025Article
- Differential regulation of BAX and BAK apoptotic activity revealed by small molecules.Science advances · 2025Article
- Article
- Comprehensive landscape of cell death mechanisms: from molecular cross-talk to therapeutic innovation in oncology.Frontiers in cell and developmental biology · 2025Review
- DLK-dependent axonal mitochondrial fission drives degeneration after axotomy.Nature communications · 2024Article
- A novel senolytic drug for pulmonary fibrosis: BTSA1 targets apoptosis of senescent myofibroblasts by activating BAX.Aging cell · 2024Article
- Covalent inhibition of pro-apoptotic BAX.Nature chemical biology · 2024Article
- Emerging connectivity of programmed cell death pathways and pulmonary vascular remodelling during pulmonary hypertension.Journal of cellular and molecular medicine · 2024Review
- The membrane insertion of the pro-apoptotic protein Bax is a Tom22-dependent multi-step process: a study in nanodiscs.Cell death discovery · 2024Article
- DLK-dependent axonal mitochondrial fission drives degeneration following axotomy.bioRxiv : the preprint server for biology · 2024Article
27 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
The BCL-2 family protein BAX is a central mediator of apoptosis. Overexpression of anti-apoptotic BCL-2 proteins contributes to tumor development and resistance to therapy by suppressing BAX and its activators. We report the discovery of BTSA1, a pharmacologically optimized BAX activator that binds with high affinity and specificity to the N-terminal activation site and induces conformational changes to BAX leading to BAX-mediated apoptosis. BTSA1-induced BAX activation effectively promotes apoptosis in leukemia cell lines and patient samples while sparing healthy cells. BAX expression levels and cytosolic conformation regulate sensitivity to BTSA1. BTSA1 potently suppressed human acute myeloid leukemia (AML) xenografts and increased host survival without toxicity. This study provides proof-of-concept for direct BAX activation as a treatment strategy in AML.
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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.