ArticleThe Journal of biological chemistry2013
Differences in the regulation of K-Ras and H-Ras isoforms by monoubiquitination.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 80 citations in OpenAlex.
- Elevated FBXL6 activates both wild-type KRAS and mutant KRASMilitary Medical Research · 2023Trial
- The Genomic Landscape of Intrinsic and Acquired Resistance to Cyclin-Dependent Kinase 4/6 Inhibitors in Patients with Hormone Receptor-Positive Metastatic Breast Cancer.Cancer discovery · 2020Trial
- Non-canonical and constitutive activation of small GTPases: more than an exception to the rule?The Biochemical journal · 2026Review
- Optimization of the Chemical Monoubiquitination System for Low-Solubility Protein: Achieving Balance Between Specificity and Yield.Current issues in molecular biology · 2026Article
- Proteomic Perspectives on KRAS-Driven Cancers and Emerging Therapeutic Approaches.Current oncology (Toronto, Ont.) · 2025Review
- The functional landscape of the human ubiquitinome.bioRxiv : the preprint server for biology · 2025Article
- Review
- Pioneer in Molecular Biology: Conformational Ensembles in Molecular Recognition, Allostery, and Cell Function.Journal of molecular biology · 2025Review
- The differential interactomes of the KRAS splice variants identify BIRC6 as a ubiquitin ligase for KRAS4A.Cell reports · 2025Article
- Review
- K128 ubiquitination constrains RAS activity by expanding its binding interface with GAP proteins.The EMBO journal · 2024Article
- Multi-monoubiquitylation controls VASP-mediated actin dynamics.Journal of cell science · 2024Article
- Lysines K117 and K147 play conserved roles in Ras activation from Drosophila to mammals.G3 (Bethesda, Md.) · 2023Article
- Regulation of Ras Signaling by S-Nitrosylation.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- Targeting small GTPases: emerging grasps on previously untamable targets, pioneered by KRAS.Signal transduction and targeted therapy · 2023Review
- The Ubiquitin-Proteasome System in Tumor Metabolism.Cancers · 2023Review
- The Four Homeostasis Knights: In Balance upon Post-Translational Modifications.International journal of molecular sciences · 2022Review
- Ubiquitylation by Rab40b/Cul5 regulates Rap2 localization and activity during cell migration.The Journal of cell biology · 2022Article
- Post-translational modification of RAS proteins.Current opinion in structural biology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Ras GTPases are signaling switches that control critical cellular processes including gene expression, differentiation, and apoptosis. The major Ras isoforms (K, H, and N) contain a conserved core GTPase domain, but have distinct biological functions. Among the three Ras isoforms there are clear differences in post-translational regulation, which contribute to differences in localization and signaling output. Modification by ubiquitination was recently reported to activate Ras signaling in cells, but the mechanisms of activation are not well understood. Here, we show that H-Ras is activated by monoubiquitination and that ubiquitination at Lys-117 accelerates intrinsic nucleotide exchange, thereby promoting GTP loading. This mechanism of Ras activation is distinct from K-Ras monoubiquitination at Lys-147, which leads to impaired regulator-mediated GTP hydrolysis. These findings reveal that different Ras isoforms are monoubiquitinated at distinct sites, with distinct mechanisms of action, but with a common ability to chronically activate the protein in the absence of a receptor signal or oncogenic mutation.
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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.