ReviewCold Spring Harbor perspectives in medicine2019
The Interdependent Activation of Son-of-Sevenless and Ras.
Review in Cold Spring Harbor perspectives in medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 72 citations in OpenAlex.
- Nintedanib inhibits the VEGFR-ERK signaling pathway in human KRAS-mutated cancer cells.Cell death & disease · 2026Article
- Mesoscale simulations of membrane-tethered reactions to parameterize cell-scale models of signaling.Biophysical journal · 2026Article
- Disrupting the KRAS-SOS1 protein-protein interaction: mechanistic rationale for pan-KRAS pathway suppression and combination therapy.Frontiers in chemistry · 2026Review
- Natural products as kinase inhibitors in lung cancer: molecular mechanisms, therapeutic potential, and clinical trials.Frontiers in pharmacology · 2026Review
- Allostery in Disease: Anticancer Drugs, Pockets, and the Tumor Heterogeneity Challenge.Journal of molecular biology · 2025Review
- Mesoscale simulations of membrane-tethered reactions to parameterize cell-scale models of signaling.bioRxiv : the preprint server for biology · 2025Article
- Evaluation of the Inhibitory Potential of Apigenin and Related Flavonoids on Various Proteins Associated with Human Diseases Using AutoDock.International journal of molecular sciences · 2025Article
- Rat Sarcoma Virus Family Genes in Acute Myeloid Leukemia: Pathogenetic and Clinical Implications.Biomedicines · 2025Review
- The roles of KRAS in cancer metabolism, tumor microenvironment and clinical therapy.Molecular cancer · 2025Review
- Influence of the gut microbiota on the pharmacokinetics of tacrolimus in liver transplant recipients: insights from microbiome analysis.Frontiers in microbiology · 2025Article
- Positive feedback in Ras activation by full-length SOS arises from autoinhibition release mechanism.Biophysical journal · 2024Article
- Making cups and rings: the 'stalled-wave' model for macropinocytosis.Biochemical Society transactions · 2024Review
- Allosteric nanobodies to study the interactions between SOS1 and RAS.Nature communications · 2024Article
- Bimodality in Ras signaling originates from processivity of the Ras activator SOS without deterministic bistability.Science advances · 2024Article
- Adapting recombinant bacterial alkaline phosphatase for nucleotide exchange of small GTPases.Protein expression and purification · 2024Article
- Membrane localization accelerates association under conditions relevant to cellular signaling.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Abl-interactor Abi suppresses the function of the BRAG2 GEF family member Schizo.Biology open · 2024Article
- Progress in Targeting KRAS Directly.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Studying early structural changes in SOS1 mediated KRAS activation mechanism.Current research in structural biology · 2024Article
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The guanine-nucleotide exchange factor (GEF) Son-of-Sevenless (SOS) plays a critical role in metazoan signaling by converting Ras•GDP (guanosine diphosphate) to Ras•GTP (guanosine triphosphate) in response to tyrosine kinase activation. Structural studies have shown that SOS differs from other Ras-specific GEFs in that SOS is itself activated by Ras•GTP binding to an allosteric site, distal to the site of nucleotide exchange. The activation of SOS involves membrane recruitment and conformational changes, triggered by lipid binding, that open the allosteric binding site for Ras•GTP. This is in contrast to other Ras-specific GEFs, which are activated by second messengers that more directly affect the active site. Allosteric Ras•GTP binding stabilizes SOS at the membrane, where it can turn over other Ras molecules processively, leading to an ultrasensitive response that is distinct from that of other Ras-specific GEFs.
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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.