ArticleScience signaling2011
Ubiquitination of K-Ras enhances activation and facilitates binding to select downstream effectors.
Article in Science signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
122 citing papers in PubMed, 185 citations in OpenAlex.
- Elevated FBXL6 activates both wild-type KRAS and mutant KRASMilitary Medical Research · 2023Trial
- Activity and specificity of KRAS variants-directed Revolution Medicines Company (RMC) compounds for pleural effusion-derived non-small cell lung cancer cell lines.Translational lung cancer research · 2026Article
- Non-canonical and constitutive activation of small GTPases: more than an exception to the rule?The Biochemical journal · 2026Review
- Mechanistic insights on spatiotemporal control of Ras-signaling.Biological chemistry · 2026Review
- USP10-mediated deubiquitination and activation ofActa pharmaceutica Sinica. B · 2026Article
- Ubiquitylation-dependent Rap2 activation regulates lamellipodia dynamics during cell migration.Journal of cell science · 2025Article
- Proteomic Perspectives on KRAS-Driven Cancers and Emerging Therapeutic Approaches.Current oncology (Toronto, Ont.) · 2025Review
- RAS-membrane interaction and oligomerization: there is more than meets the eye.Biochemical Society transactions · 2025Review
- Review
- The differential interactomes of the KRAS splice variants identify BIRC6 as a ubiquitin ligase for KRAS4A.Cell reports · 2025Article
- Review
- Rap1 activity and localization is regulated by Rab40/CRL5 facilitated mono-ubiquitylation.microPublication biology · 2025Article
- New insights into protein-protein interaction modulators in drug discovery and therapeutic advance.Signal transduction and targeted therapy · 2024Review
- Pharmacological targeting of casein kinase 1δ suppresses oncogenic NRAS-driven melanoma.Nature communications · 2024Article
- KCTD17-mediated Ras stabilization promotes hepatocellular carcinoma progression.Clinical and molecular hepatology · 2024Article
- Functional and structural insights into RAS effector proteins.Molecular cell · 2024Review
- A Bioinformatic Analysis Predicts That Cannabidiol Could Function as a Potential Inhibitor of the MAPK Pathway in Colorectal Cancer.Current issues in molecular biology · 2024Article
- CALU promotes lung adenocarcinoma progression by enhancing cell proliferation, migration and invasion.Respiratory research · 2024Article
- K128 ubiquitination constrains RAS activity by expanding its binding interface with GAP proteins.The EMBO journal · 2024Article
- Cross-family small GTPase ubiquitination by the intracellular pathogenMolecular biology of the cell · 2024Article
62 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The guanosine triphosphate (GTP)--loaded form of the guanosine triphosphatase (GTPase) Ras initiates multiple signaling pathways by binding to various effectors, such as the kinase Raf and phosphatidylinositol 3-kinase (PI3K). Ras activity is increased by guanine nucleotide exchange factors that stimulate guanosine diphosphate release and GTP loading and is inhibited by GTPase-activating proteins that stimulate GTP hydrolysis. KRAS is the most frequently mutated RAS gene in cancer. Here, we report that monoubiquitination of lysine-147 in the guanine nucleotide-binding motif of wild-type K-Ras could lead to enhanced GTP loading. Furthermore, ubiquitination increased the binding of the oncogenic Gly12Val mutant of K-Ras to the downstream effectors PI3K and Raf. Thus, monoubiquitination could enhance GTP loading on K-Ras and increase its affinity for specific downstream effectors, providing a previously unidentified mechanism for Ras activation.
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What OpenQuestion holds
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.