ArticleProceedings of the National Academy of Sciences of the United States of America2019
BCL-2 family protein BOK is a positive regulator of uridine metabolism in mammals.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Loss of BOK increases vulnerability of p53 deficient non-small cell lung cancer cells to ATR inhibition through its role in uridine metabolism.Cell death and differentiation · 2026Article
- BOK beyond apoptosis: pyrimidine metabolism and ATR dependence in p53-deficient lung cancer.Cell death and differentiation · 2026Article
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- Low BOK Expression Promotes Epithelial-Mesenchymal Transition and Migration via the Wnt Signaling Pathway in Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Olaparib increases chemosensitivity by upregulating miR-125a-3p in ovarian cancer cells.Discover oncology · 2025Article
- Molecular Cell Biology of Apoptosis in Health and Disease.Advances in experimental medicine and biology · 2025Review
- GPX3-Mediated Oxidative Stress Affects Pyrimidine Metabolism Levels in Stomach Adenocarcinoma via the AMPK/mTOR Pathway.International journal of clinical practice · 2024Article
- Identification of Potential Genes and Critical Pathways in Postoperative Recurrence of Crohn's Disease by Machine Learning And WGCNA Network Analysis.Current genomics · 2023Article
- Article
- Bok: real killer or bystander with non-apoptotic roles?Frontiers in cell and developmental biology · 2023Review
- Human β-Defensin 2 (HBD-2) Displays Oncolytic Activity but Does Not Affect Tumour Cell Migration.Biomolecules · 2022Article
- The BCL-2 family member BOK promotes KRAS-driven lung cancer progression in a p53-dependent manner.Oncogene · 2022Article
- Endogenous Bok is stable at the endoplasmic reticulum membrane and does not mediate proteasome inhibitor-induced apoptosis.Frontiers in cell and developmental biology · 2022Article
- Blood transcriptomics identifies immune signatures indicative of infectious complications in childhood cancer patients with febrile neutropenia.Clinical & translational immunology · 2022Article
- The BH3-only protein NOXA serves as an independent predictor of breast cancer patient survival and defines susceptibility to microtubule targeting agents.Cell death & disease · 2021Article
- Recent Updates on Mechanisms of Resistance to 5-Fluorouracil and Reversal Strategies in Colon Cancer Treatment.Biology · 2021Review
- Loss of BOK Has a Minor Impact on Acetaminophen Overdose-Induced Liver Damage in Mice.International journal of molecular sciences · 2021Article
- Yes, MAM!Molecular & cellular oncology · 2021Article
- Identification of the Bok Interactome Using Proximity Labeling.Frontiers in cell and developmental biology · 2021Article
- The Mysteries around the BCL-2 Family Member BOK.Biomolecules · 2020Review
Corrections and comments
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Authors and funding
25 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BCL-2 family proteins regulate the mitochondrial apoptotic pathway. BOK, a multidomain BCL-2 family protein, is generally believed to be an adaptor protein similar to BAK and BAX, regulating the mitochondrial permeability transition during apoptosis. Here we report that BOK is a positive regulator of a key enzyme involved in uridine biosynthesis; namely, uridine monophosphate synthetase (UMPS). Our data suggest that BOK expression enhances UMPS activity, cell proliferation, and chemosensitivity. Genetic deletion of
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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.