ArticleScience advances2024
Cysteamine dioxygenase (ADO) governs cancer cell mitochondrial redox homeostasis through proline metabolism.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Metabolites and cancer metastasis.Oncogene · 2026Review
- Multifunctional biohybrid nanoplatform interferes electron transport chain amplifying mitochondrial metabolism-mediated anti-tumor therapy.Materials today. Bio · 2026Article
- Genistein Protects Against Lead-Induced Cognitive Impairment Through a Glutathione-Dependent Redox-Mitochondrial Apoptosis Axis.Molecules (Basel, Switzerland) · 2026Article
- Structural Principles of Covalent Flavin Modification in Oxidoreductases.Biochemistry · 2026Review
- Pan-Cancer Landscape of the Novel Oxygen Sensor ADO and Its Potential Role in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Article
- Hydralazine inhibits cysteamine dioxygenase to treat preeclampsia and senesce glioblastoma.Science advances · 2025Article
- Global profiling of N-terminal cysteine-dependent degradation mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- An mRNA-display derived cyclic peptide scaffold reveals the substrate binding interactions of an N-terminal cysteine oxidase.Nature communications · 2025Article
- Taurine and proline promote lung tumour growth by co-regulating Azgp1/mTOR signalling pathway.NPJ precision oncology · 2025Article
- Hydralazine inhibits cysteamine dioxygenase to treat preeclampsia and senesce glioblastoma.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
2-Aminoethanethiol dioxygenase (ADO) is a thiol dioxygenase that sulfinylates cysteamine and amino-terminal cysteines in polypeptides. The pathophysiological roles of ADO remain largely unknown. Here, we demonstrate that ADO expression represents a vulnerability in cancer cells, as ADO depletion led to loss of proliferative capacity and survival in cancer cells and reduced xenograft growth. In contrast, generation of the
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