ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Nuclear Control of Mitochondrial Homeostasis and Venetoclax Efficacy in AML via COX4I1.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
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Who cites it
6 citing papers in PubMed.
- Transcriptomic profiling and structural characterization reveal UQCRC1 and COX4I1 as key mitochondrial regulators associated with oxidative stress in multiple sclerosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Localized heme sensing through a ternary molecular glue.bioRxiv : the preprint server for biology · 2026Article
- Functional and Molecular Characterization of Melamine-Induced Disruption of Human Spermatozoa via Oxidative Stress and Apoptotic Pathways: An In Vitro Study.Antioxidants (Basel, Switzerland) · 2026Article
- Nuclear Control of Mitochondrial Homeostasis and Venetoclax Efficacy in AML via COX4I1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integration of single-cell and bulk RNA sequencing to identify unique tumor stem cells and construct novel prognostic markers for assessing ESCA prognosis and drug sensitivity.Frontiers in oncology · 2025Article
- The Nuclear-Encoded Cytochrome c Oxidase Subunit COX4-1 Enhances Hypoxia Tolerance in Glioblastoma Cells.Journal of oncology research and therapy · 2025Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Cell signaling pathways are enriched for biological processes crucial for cellular communication, response to external stimuli, and metabolism. Here, a cell signaling-focused CRISPR screen identified cytochrome c oxidase subunit 4 isoform 1 (COX4I1) as a novel vulnerability in acute myeloid leukemia (AML). Depletion of COX4I1 hindered leukemia cell proliferation and impacted in vivo AML progression. Mechanistically, loss of COX4I1 induced mitochondrial stress and ferroptosis, disrupting mitochondrial ultrastructure and oxidative phosphorylation. CRISPR gene tiling scans, coupled with mitochondrial proteomics, dissected critical regions within COX4I1 essential for leukemia cell survival, providing detailed insights into the mitochondrial Complex IV assembly network. Furthermore, COX4I1 depletion or pharmacological inhibition of Complex IV (using chlorpromazine) synergized with venetoclax, providing a promising avenue for improved leukemia therapy. This study highlights COX4I1, a nuclear encoded mitochondrial protein, as a critical mitochondrial checkpoint, offering insights into its functional significance and potential clinical implications 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.