ArticleMolecular and cellular biology2015
The ubiquitin E3 ligase SCF-FBXO24 recognizes deacetylated nucleoside diphosphate kinase A to enhance its degradation.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Nucleoside diphosphate kinase strongly promotes GDP and ADP metabolism in the cell and affects endogenous proton leak in mitochondria - the kinase is hampered by oxidative phosphorylation inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Ivabradine induces RAD51 degradation, potentiating PARP inhibitor efficacy in non-germline BRCA pathogenic variant triple-negative breast cancer.Journal of translational medicine · 2025Article
- Reciprocal Regulation Between the SCFbioRxiv : the preprint server for biology · 2025Article
- Targeted degradation of extracellular mitochondrial aspartyl-tRNA synthetase modulates immune responses.Nature communications · 2024Article
- FOXK2 targeting by the SCF-E3 ligase subunit FBXO24 for ubiquitin mediated degradation modulates mitochondrial respiration.The Journal of biological chemistry · 2024Article
- PRUNE1 and NME/NDPK family proteins influence energy metabolism and signaling in cancer metastases.Cancer metastasis reviews · 2024Review
- Article
- Heat-shock protein 90α protects NME1 against degradation and suppresses metastasis of breast cancer.British journal of cancer · 2023Article
- Elucidation of TRIM25 ubiquitination targets involved in diverse cellular and antiviral processes.PLoS pathogens · 2022Article
- Identification of immune-related endoplasmic reticulum stress genes in sepsis using bioinformatics and machine learning.Frontiers in immunology · 2022Article
- Regulation of metastasis suppressor NME1 by a key metabolic cofactor coenzyme A.Redox biology · 2021Article
- Loss of the Metastasis Suppressor NME1, But Not of Its Highly Related Isoform NME2, Induces a Hybrid Epithelial-Mesenchymal State in Cancer Cells.International journal of molecular sciences · 2021Article
- A Fbxo48 inhibitor prevents pAMPKα degradation and ameliorates insulin resistance.Nature chemical biology · 2021Article
- Mutations at the dimer interface and surface residues of Nm23-H1 metastasis suppressor affect its expression and function.Molecular and cellular biochemistry · 2020Article
- The Function of NM23-H1/NME1 and Its Homologs in Major Processes Linked to Metastasis.Pathology oncology research : POR · 2020Review
- Cand1-Mediated Adaptive Exchange Mechanism Enables Variation in F-Box Protein Expression.Molecular cell · 2018Article
- The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Lipopolysaccharide modulates p300 and Sirt1 to promote PRMT1 stability via an SCFJournal of cell science · 2017Article
- Post-translational modification of the interferon-gamma receptor alters its stability and signaling.The Biochemical journal · 2017Article
- Oxidative stress destabilizes protein arginine methyltransferase 4 via glycogen synthase kinase 3β to impede lung epithelial cell migration.American journal of physiology. Cell physiology · 2017Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The Skp-Cul-F box (SCF) ubiquitin E3 ligase machinery recognizes predominantly phosphodegrons or, less commonly, an (I/L)Q molecular signature within substrates to facilitate their recruitment in mediating protein ubiquitination and degradation. Here, we examined the molecular signals that determine the turnover of the multifunctional enzyme nucleoside diphosphate kinase A (NDPK-A) that controls cell proliferation. NDPK-A protein exhibits a half-life of ∼6 h in HeLa cells and is targeted for ubiquitylation through actions of the F-box protein FBXO24. SCF-FBXO24 polyubiquitinates NDPK-A at K85, and two NH(2)-terminal residues, L55 and K56, were identified as important molecular sites for FBXO24 interaction. Importantly, K56 acetylation impairs its interaction with FBXO24, and replacing K56 with Q56, an acetylation mimic, reduces NDPK-A FBXO24 binding capacity. The acetyltransferase GCN5 catalyzes K56 acetylation within NDPK-A, thereby stabilizing NDPK-A, whereas GCN5 depletion in cells accelerates NDPK-A degradation. Cellular expression of an NDPK-A acetylation mimic or FBXO24 silencing increases NDPK-A life span which, in turn, impairs cell migration and wound healing. We propose that lysine acetylation when presented in the appropriate context may be recognized by some F-box proteins as a unique inhibitory molecular signal for their recruitment to restrict substrate degradation.
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