ArticleCell2025
GUK1 activation is a metabolic liability in lung cancer.
Article in Cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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Who cites it
15 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Mass spectrometry-based human spatial omics: fundamentals, innovations, and applications.Journal of biomedical science · 2026Pooled it
- Global research trends and emerging themes in amino acid deprivation based cancer therapy: a bibliometric and visualization study.Frontiers in immunology · 2026Pooled it
- Proteomic investigation of signaling dynamics: from static maps to network rewiring.Bioscience reports · 2026Review
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- Dynamic control of nucleotide metabolism in physiology and disease.Nature cell biology · 2026Review
- Proteome-Transcriptome Discordance in Rice Under Drought Is Modulated by Post-Translational Modifications with Functional Consequences for Photosynthesis and Energy Metabolism.Plants (Basel, Switzerland) · 2026Article
- 5' UTR length shapes alternative N-terminal protein isoforms across cancers and in rare disease.EMBO reports · 2026Article
- The oncogenic control of nucleotide synthesis.Oncogenesis · 2026Review
- The 2025 lung cancer landscape: advances in screening, molecular taxonomy and therapeutic strategy: a narrative review.Translational lung cancer research · 2026Review
- Dynamic Monitoring of Content Variation of Guanosine Triphosphate in Single Cells under External Stimulus with Functionalized Fluorescent/Photothermal NbChemical & biomedical imaging · 2026Article
- Spatial mapping of CoQ10 repletion by BPM31510 in a genetic mouse model (Coq4Journal of lipid research · 2026Article
- 5' UTR length regulates alternative N-terminal protein isoform production in health and disease.bioRxiv : the preprint server for biology · 2026Article
- Proteomic Analysis of PTEN-Deficient Cells Reveals Src-Mediated Upregulation of EphA2 and Therapeutic Potential of Dual Inhibition.Molecular & cellular proteomics : MCP · 2025Article
- Focal adhesion kinase/Src family kinase axis-mediated tyrosine phosphorylation of metabolic enzymes facilitates tumor metastasis.Signal transduction and targeted therapy · 2025Article
- Post-translational modifications and the reprogramming of tumor metabolism.Discover oncology · 2025Review
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
Little is known about metabolic vulnerabilities in oncogene-driven lung cancer. Here, we perform a phosphoproteomic screen in anaplastic lymphoma kinase (ALK)-rearranged ("ALK+") patient-derived cell lines and identify guanylate kinase 1 (GUK1), a guanosine diphosphate (GDP)-synthesizing enzyme, as a target of ALK signaling in lung cancer. We demonstrate that ALK binds to and phosphorylates GUK1 at tyrosine 74 (Y74), resulting in increased GDP biosynthesis. Spatial imaging of ALK+ patient tumor specimens shows enhanced phosphorylation of GUK1 that significantly correlates with guanine nucleotides in situ. Abrogation of GUK1 phosphorylation reduces intracellular GDP and guanosine triphosphate (GTP) pools and decreases mitogen-activated protein kinase (MAPK) signaling and Ras-GTP loading. A GUK1 variant that cannot be phosphorylated (Y74F) decreases tumor proliferation in vitro and in vivo. Beyond ALK, other oncogenic fusion proteins in lung cancer also regulate GUK1 phosphorylation. These studies may pave the way for the development of new therapeutic approaches by exploiting metabolic dependencies in oncogene-driven lung cancers.
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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.