ArticleNature structural & molecular biology2016
One-way membrane trafficking of SOS in receptor-triggered Ras activation.
Article in Nature structural & molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 63 citations in OpenAlex.
- Mimicking Cellular Membranes With Micropatterned Lipid Bilayers.Chemphyschem : a European journal of chemical physics and physical chemistry · 2026Article
- Mutant and Wild-Type RAS Cross-talk and Stoichiometric Deficiencies Are Determinants of Sensitivity to Targeted Therapies in KRASG12R Pancreatic Ductal Adenocarcinoma.Cancer research · 2026Article
- Disrupting the KRAS-SOS1 protein-protein interaction: mechanistic rationale for pan-KRAS pathway suppression and combination therapy.Frontiers in chemistry · 2026Review
- Molecular Frameworks for ERK1/2 Inhibition: Lessons from Synthetic and SAR Explorations.ACS omega · 2025Review
- Enzymatic Reactions Dictated by the 2D Membrane Environment.The journal of physical chemistry letters · 2025Article
- In Silico Identification of Putative Allosteric Pockets and Inhibitors for the KRASG13D-SOS1 Complex in Cancer Therapy.International journal of molecular sciences · 2025Article
- RAS signaling in carcinogenesis, cancer therapy and resistance mechanisms.Journal of hematology & oncology · 2024Review
- Positive feedback in Ras activation by full-length SOS arises from autoinhibition release mechanism.Biophysical journal · 2024Article
- Bimodality in Ras signaling originates from processivity of the Ras activator SOS without deterministic bistability.Science advances · 2024Article
- GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer.Nature communications · 2024Article
- Mediating kinase activity in Ras-mutant cancer: potential for an individualised approach?Frontiers in pharmacology · 2024Review
- Two-dimensional molecular condensation in cell signaling and mechanosensing.Acta biochimica et biophysica Sinica · 2023Review
- Micropatterning of functional lipid bilayer assays for quantitative bioanalysis.Biomicrofluidics · 2023Article
- PPDPF Promotes the Development of Mutant KRAS-Driven Pancreatic Ductal Adenocarcinoma by Regulating the GEF Activity of SOS1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Competition for shared downstream signaling molecules establishes indirect negative feedback between EGFR and EphA2.Biophysical journal · 2022Article
- A two-component protein condensate of the EGFR cytoplasmic tail and Grb2 regulates Ras activation by SOS at the membrane.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Subcellular Dynamic Immunopatterning of Cytosolic Protein Complexes on Microstructured Polymer Substrates.ACS sensors · 2021Article
- Stochasticity and positive feedback enable enzyme kinetics at the membrane to sense reaction size.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Relating cellular signaling timescales to single-molecule kinetics: A first-passage time analysis of Ras activation by SOS.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Membrane anchoring facilitates colocalization of enzymes in plant cytochrome P450 redox systems.Communications biology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
SOS is a key activator of the small GTPase Ras. In cells, SOS-Ras signaling is thought to be initiated predominantly by membrane recruitment of SOS via the adaptor Grb2 and balanced by rapidly reversible Grb2-SOS binding kinetics. However, SOS has multiple protein and lipid interactions that provide linkage to the membrane. In reconstituted-membrane experiments, these Grb2-independent interactions were sufficient to retain human SOS on the membrane for many minutes, during which a single SOS molecule could processively activate thousands of Ras molecules. These observations raised questions concerning how receptors maintain control of SOS in cells and how membrane-recruited SOS is ultimately released. We addressed these questions in quantitative assays of reconstituted SOS-deficient chicken B-cell signaling systems combined with single-molecule measurements in supported membranes. These studies revealed an essentially one-way trafficking process in which membrane-recruited SOS remains trapped on the membrane and continuously activates Ras until being actively removed via endocytosis.
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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.