ArticleSmall GTPases
Site-specific monoubiquitination activates Ras by impeding GTPase-activating protein function.
Article in Small GTPases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The differential interactomes of the KRAS splice variants identify BIRC6 as a ubiquitin ligase for KRAS4A.Cell reports · 2025Article
- Lysines K117 and K147 play conserved roles in Ras activation from Drosophila to mammals.G3 (Bethesda, Md.) · 2023Article
- Post-translational modification of RAS proteins.Current opinion in structural biology · 2021Review
- Divergent Mechanisms Activating RAS and Small GTPases Through Post-translational Modification.Frontiers in molecular biosciences · 2021Review
- A conserved, N-terminal tyrosine signal directs Ras for inhibition by Rabex-5.PLoS genetics · 2020Article
- RAS ubiquitylation modulates effector interactions.Small GTPases · 2020Article
- Biology, pathology, and therapeutic targeting of RAS.Advances in cancer research · 2020Review
- Regulation of large and small G proteins by ubiquitination.The Journal of biological chemistry · 2019Review
- A simple toolset to identify endogenous post-translational modifications for a target protein: a snapshot of the EGFR signaling pathway.Bioscience reports · 2017Article
- New ligation independent cloning vectors for expression of recombinant proteins with a self-cleaving CPD/6xHis-tag.BMC biotechnology · 2017Article
- The structural basis for cancer treatment decisions.Oncotarget · 2014Review
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Authors and funding
4 authors.
Funding
Abstract
KRas has recently been shown to be activated by monoubiquitination (mUb). Similar to oncogenic mutations, mUb of Ras at position 147 activates Ras by causing a defect in GTPase activating protein (GAP) function. To characterize the mechanism by which mUb impairs GAP-mediated downregulation of Ras, we made various modifications at position 147 of Ras and examined the impact on Ras sensitivity to GAP function. Whereas small modifications (iodoacetamide and glutathione) at position 147 of Ras do not affect GAP-mediated hydrolysis, ligation of Ras to Ub(G76C) (native linker), Ub(X77C) (one residue longer), and PDZ2 (with a native ubiquitin linker) was defective in GAP-mediated GTP hydrolysis. However, restoration of GAP activity was observed for Ras modified with the PDZ2 domain containing a shorter and stiffer linker region than ubiquitin. Therefore, the properties of the linker region dictate whether modification affects GAP-mediated hydrolysis, and our data indicate that the GAP defect requires a minimum linker length of 7 to 8 residues.
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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.