ArticleProceedings of the National Academy of Sciences of the United States of America2014
Src promotes GTPase activity of Ras via tyrosine 32 phosphorylation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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.
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Who cites it
69 citing papers in PubMed, 102 citations in OpenAlex.
- RinPy, a Python Package for Residue Interaction Network Model to Analyze Protein Structures and Predict Ligand Binding Sites.Journal of chemical information and modeling · 2026Article
- Mechanistic insights on spatiotemporal control of Ras-signaling.Biological chemistry · 2026Review
- Posttranslational modifications remodel proteome-wide ligandability.Nature chemical biology · 2026Article
- Decoding the Post-translational Modification Crosstalk: Functional Implications of Phosphorylation, Acetylation, and Methylation.The journal of physical chemistry. B · 2026Article
- Deciphering the Interlinked CXCR4-Mediated Feedback Loop Among Signaling Pathways in Diabetic Wound Healing.Current diabetes reviews · 2026Review
- Synergistic Inhibition of Drug Resistant KRAS Mutant Non-Small Cell Lung Cancer by Co-Targeting AXL and SRC.Cancers · 2025Article
- Unraveling the mechanisms of antitumor action ofIn silico pharmacology · 2025Article
- Oscillatory dynamics of Rac1 activity in Dictyostelium discoideum amoebae.PLoS computational biology · 2024Article
- MYC and KRAS cooperation: from historical challenges to therapeutic opportunities in cancer.Signal transduction and targeted therapy · 2024Review
- Tirbanibulin decreases cell proliferation and downregulates protein expression of oncogenic pathways in human papillomavirus containing HeLa cells.Archives of dermatological research · 2024Article
- Molecular Mechanism of Phosphorylation-Mediated Impacts on the Conformation Dynamics of GTP-Bound KRAS Probed by GaMD Trajectory-Based Deep Learning.Molecules (Basel, Switzerland) · 2024Article
- Genetically encodable biosensors for Ras activity.RSC chemical biology · 2024Review
- Far-reaching effects of tyrosine64 phosphorylation on Ras revealed with BeFCommunications chemistry · 2024Article
- Logic-based mechanistic machine learning on high-content images reveals how drugs differentially regulate cardiac fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Logic-based mechanistic machine learning on high-content images reveals how drugs differentially regulate cardiac fibroblasts.bioRxiv : the preprint server for biology · 2023Article
- Regulation of Ras Signaling by S-Nitrosylation.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- Functional roles of SRC signaling in pancreatic cancer: Recent insights provide novel therapeutic opportunities.Oncogene · 2023Review
- Targeting small GTPases: emerging grasps on previously untamable targets, pioneered by KRAS.Signal transduction and targeted therapy · 2023Review
- Sex differences in synaptic plasticity underlying learning.Journal of neuroscience research · 2023Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Mutations in Ras GTPase and various other components of the Ras signaling pathways are among the most common genetic alterations in human cancers and also have been identified in several familial developmental syndromes. Over the past few decades it has become clear that the activity or the oncogenic potential of Ras is dependent on the nonreceptor tyrosine kinase Src to promote the Ras/Raf/MAPK pathway essential for proliferation, differentiation, and survival of eukaryotic cells. However, no direct relationship between Ras and Src has been established. We show here that Src binds to and phosphorylates GTP-, but not GDP-, loaded Ras on a conserved Y32 residue within the switch I region in vitro and that in vivo, Ras-Y32 phosphorylation markedly reduces the binding to effector Raf and concomitantly increases binding to GTPase-activating proteins and the rate of GTP hydrolysis. These results suggest that, in the context of predetermined crystallographic structures, Ras-Y32 serves as an Src-dependent keystone regulatory residue that modulates Ras GTPase activity and ensures unidirectionality to the Ras GTPase cycle.
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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.