ArticleThe Journal of biological chemistry2010
Activation of the Ran GTPase is subject to growth factor regulation and can give rise to cellular transformation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Genetic landscape of congenital pouch colon: systematic review and functional enrichment study.Pediatric surgery international · 2024Pooled it
- Engineering an orthogonal ubiquitin transfer cascade with RING E3 RNF38 by phage display to reveal its regulation of nuclear transport.The Journal of biological chemistry · 2026Article
- Induced opening of conformational switch I in GTP-bound Ran GTPase.Protein science : a publication of the Protein Society · 2026Article
- The Small GTPase Ran Increases Sensitivity of Ovarian Cancer Cells to Oncolytic Vesicular Stomatitis Virus.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Computational approach for decoding malaria drug targets from single-cell transcriptomics and finding potential drug molecule.Scientific reports · 2024Article
- The Nuclear Cap-Binding Complex, a multitasking binding partner of RNA polymerase II transcripts.Journal of biochemistry · 2023Review
- Ran GTPase and Its Importance in Cellular Signaling and Malignant Phenotype.International journal of molecular sciences · 2023Review
- High expression of Ran binding protein 1 predicts poor outcomes in hepatocellular carcinoma patients: a Cancer Genome Atlas database analysis.Journal of gastrointestinal oncology · 2021Article
- Active GTPase Pulldown Protocol.Methods in molecular biology (Clifton, N.J.) · 2021Article
- GEF-independent Ran activation shifts a fraction of the protein to the cytoplasm and promotes cell proliferation.Molecular biomedicine · 2020Article
- Computational inference of cancer-specific vulnerabilities in clinical samples.Genome biology · 2020Article
- Ran GTPase: A Key Player in Tumor Progression and Metastasis.Frontiers in cell and developmental biology · 2020Review
- Ran promotes membrane targeting and stabilization of RhoA to orchestrate ovarian cancer cell invasion.Nature communications · 2019Article
- The coming-of-age of nucleocytoplasmic transport in motor neuron disease and neurodegeneration.Cellular and molecular life sciences : CMLS · 2019Review
- Trophinin-associated protein expression is an independent prognostic biomarker in lung adenocarcinoma.Journal of thoracic disease · 2019Article
- Identification and Expression Profiling of theInternational journal of molecular sciences · 2019Article
- Novel Ran-RCC1 Inhibitory Peptide-Loaded Nanoparticles Have Anti-Cancer Efficacy In Vitro and In Vivo.Cancers · 2019Article
- Knockdown of Ran GTPase expression inhibits the proliferation and migration of breast cancer cells.Molecular medicine reports · 2018Article
- Downregulated Trophinin-Associated Protein Plays a Critical Role in Human Hepatocellular Carcinoma Through Upregulation of Tumor Cell Growth and Migration.Oncology research · 2018Article
- Overexpressed genes in malignant pleural mesothelioma: implications in clinical management.Journal of thoracic disease · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Although the small GTPase Ran is best known for its roles in nucleocytoplasmic transport, mitotic spindle assembly, and nuclear envelope formation, recent studies have demonstrated the overexpression of Ran in multiple tumor types and that its expression is correlated with a poor patient prognosis, providing evidence for the importance of this GTPase in cell growth regulation. Here we show that Ran is subject to growth factor regulation by demonstrating that it is activated in a serum-dependent manner in human breast cancer cells and, in particular, in response to heregulin, a growth factor that activates the Neu/ErbB2 tyrosine kinase. The heregulin-dependent activation of Ran requires mTOR (mammalian target of rapamycin) and stimulates the capped RNA binding capability of the cap-binding complex in the nucleus, thus influencing gene expression at the level of mRNA processing. We further demonstrate that the excessive activation of Ran has important consequences for cell growth by showing that a novel, activated Ran mutant is sufficient to transform NIH-3T3 cells in an mTOR- and epidermal growth factor receptor-dependent manner and that Ran-transformed cells form tumors in mice.
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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.