ArticleProceedings of the National Academy of Sciences of the United States of America2019
M-Ras/Shoc2 signaling modulates E-cadherin turnover and cell-cell adhesion during collective cell migration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- SHOC2 Is a Novel Cause of Central Conducting Lymphatic Anomaly.American journal of medical genetics. Part A · 2026Article
- Expression of LIFR in tumor and SHOC2, YAP1 in plasma mRNA as potential biomarkers in KRASScientific reports · 2026Article
- Metabolic maintenance of breast cancer cells and metastases through E-cadherin/YAP-dependent pyruvate carboxylase expression.bioRxiv : the preprint server for biology · 2026Article
- Gene variants in periventricular nodular heterotopia.Acta epileptologica · 2026Review
- A naturally synonymous mutation modulates an ERK-centered regulatory network to mediate thermotolerance divergence in Crassostrea oysters.Communications biology · 2026Article
- Antagonists of the N-cadherin/Fibroblast growth factor receptor tyrosine kinase complex.Tissue barriers · 2026Review
- Epigenetic-mediated positive feedback loop facilitates the progression of lung adenocarcinoma.iScience · 2025Article
- Progress of KRAS G12C inhibitors in the treatment of refractory colorectal cancer and strategies for drug resistance response.Investigational new drugs · 2025Review
- A Modified Tridecapeptide Probe for Imaging Cell Junction.Molecules (Basel, Switzerland) · 2024Article
- Identification of Mitophagy-Associated Genes for the Prediction of Metabolic Dysfunction-Associated Steatohepatitis Based on Interpretable Machine Learning Models.Journal of inflammation research · 2024Article
- Structural insights into the role of SHOC2-MRAS-PP1C complex in RAF activation.The FEBS journal · 2023Review
- Scribble mis-localization induces adaptive resistance to KRAS G12C inhibitors through feedback activation of MAPK signaling mediated by YAP-induced MRAS.Nature cancer · 2023Article
- Shoc2 controls ERK1/2-driven neural crest development by balancing components of the extracellular matrix.Developmental biology · 2022Article
- Structure of the SHOC2-MRAS-PP1C complex provides insights into RAF activation and Noonan syndrome.Nature structural & molecular biology · 2022Article
- Expanding the molecular spectrum of pathogenic SHOC2 variants underlying Mazzanti syndrome.Human molecular genetics · 2022Article
- Potential Therapeutic Applications of N-Cadherin Antagonists and Agonists.Frontiers in cell and developmental biology · 2022Review
- NSUN2 modified by SUMO-2/3 promotes gastric cancer progression and regulates mRNA m5C methylation.Cell death & disease · 2021Article
- A Leucine-Rich Repeat Protein Provides a SHOC2 the RAS Circuit: a Structure-Function Perspective.Molecular and cellular biology · 2021Review
- A requirement for p120-catenin in the metastasis of invasive ductal breast cancer.Journal of cell science · 2021Article
- The leucine-rich repeat signaling scaffolds Shoc2 and Erbin: cellular mechanism and role in disease.The FEBS journal · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Collective cell migration is required for normal embryonic development and contributes to various biological processes, including wound healing and cancer cell invasion. The M-Ras GTPase and its effector, the Shoc2 scaffold, are proteins mutated in the developmental RASopathy Noonan syndrome, and, here, we report that activated M-Ras recruits Shoc2 to cell surface junctions where M-Ras/Shoc2 signaling contributes to the dynamic regulation of cell-cell junction turnover required for collective cell migration. MCF10A cells expressing the dominant-inhibitory M-Ras
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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.