ArticlePloS one2016
The RAS-Effector Interface: Isoform-Specific Differences in the Effector Binding Regions.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 75 citations in OpenAlex.
- G12 mutations rewire allosteric communication at the Ras-RalGDS interface.Biophysical journal · 2026Article
- Synthesis and Biochemical Characterization of Investigational Pyrazolopyrimidine-Based Allosteric KRAS Modulators.ACS medicinal chemistry letters · 2026Article
- Protein-based pan-RAS inhibitor induces tumor regression in female mice via IFNγ and CD8Nature communications · 2026Article
- Revisiting RAS family GTPase signaling: effector selectivity and oncogenic bypass.The Biochemical journal · 2026Review
- An evolutionarily conserved salt bridge stabilizes the active site for GTP hydrolysis in Rho GTPases.The Journal of biological chemistry · 2026Article
- KRAS4a and KRAS4b show distinct lipid-dependent regulation of RAS-RAF membrane dynamics.The Journal of biological chemistry · 2026Article
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- Review
- A nucleotide-independent, pan-RAS-targeted DARPin elicits anti-tumor activity in a multimodal manner.Molecular oncology · 2025Article
- Integrative analysis of RAS signaling effectors reveals stage-dependent oncogenic patterns in colon adenocarcinoma.Biotechnology reports (Amsterdam, Netherlands) · 2025Article
- Recent advances in targeted degradation in the RAS pathway.Future medicinal chemistry · 2025Review
- Distinct association of HRAS and KRAS with MnMagnetic resonance letters · 2025Article
- Structural insights into isoform-specific RAS-PI3Kα interactions and the role of RAS in PI3Kα activation.Nature communications · 2025Article
- Functional and structural insights into RAS effector proteins.Molecular cell · 2024Review
- RAS and SHOC2 Roles in RAF Activation and Therapeutic Considerations.Annual review of cancer biology · 2024Article
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- RAS-dependent RAF-MAPK hyperactivation by pathogenic RIT1 is a therapeutic target in Noonan syndrome-associated cardiac hypertrophy.Science advances · 2023Article
- RAS pathway: The new frontier of brain mosaicism in epilepsy.Neurobiology of disease · 2023Review
- Editorial: Identifying the isoform-specific roles of RAS paralogs in health and disease.Frontiers in cell and developmental biology · 2023Article
- Peptidomimetics designed to bind to RAS effector domain are promising cancer therapeutic compounds.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RAS effectors specifically interact with the GTP-bound form of RAS in response to extracellular signals and link them to downstream signaling pathways. The molecular nature of effector interaction by RAS is well-studied but yet still incompletely understood in a comprehensive and systematic way. Here, structure-function relationships in the interaction between different RAS proteins and various effectors were investigated in detail by combining our in vitro data with in silico data. Equilibrium dissociation constants were determined for the binding of HRAS, KRAS, NRAS, RRAS1 and RRAS2 to both the RAS binding (RB) domain of CRAF and PI3Kα, and the RAS association (RA) domain of RASSF5, RALGDS and PLCε, respectively, using fluorescence polarization. An interaction matrix, constructed on the basis of available crystal structures, allowed identification of hotspots as critical determinants for RAS-effector interaction. New insights provided by this study are the dissection of the identified hotspots in five distinct regions (R1 to R5) in spite of high sequence variability not only between, but also within, RB/RA domain-containing effectors proteins. Finally, we propose that intermolecular β-sheet interaction in R1 is a central recognition region while R3 may determine specific contacts of RAS versus RRAS isoforms with effectors.
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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.