ArticleCellular signalling2016
Shoc2-tranduced ERK1/2 motility signals--Novel insights from functional genomics.
Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Gene variants in periventricular nodular heterotopia.Acta epileptologica · 2026Review
- Article
- Signalling pathways involved in urotensin II induced ventricular myocyte hypertrophy.PloS one · 2025Article
- SHOC2 plays an oncogenic or tumor-suppressive role by differentially targeting the MAPK and mTORC1 signals in liver cancer.Life medicine · 2024Article
- Article
- Shoc2 controls ERK1/2-driven neural crest development by balancing components of the extracellular matrix.Developmental biology · 2022Article
- The leucine-rich repeat signaling scaffolds Shoc2 and Erbin: cellular mechanism and role in disease.The FEBS journal · 2021Review
- Single-domain antibodies for functional targeting of the signaling scaffold Shoc2.Molecular immunology · 2020Article
- SHOC2 is associated with the survival of breast cancer cells and has prognostic value for patients with breast cancer.Molecular medicine reports · 2020Article
- The FBXW7-SHOC2-Raptor Axis Controls the Cross-Talks between the RAS-ERK and mTORC1 Signaling Pathways.Cell reports · 2019Article
- M-Ras/Shoc2 signaling modulates E-cadherin turnover and cell-cell adhesion during collective cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Hematopoietic and neural crest defects in zebrafish shoc2 mutants: a novel vertebrate model for Noonan-like syndrome.Human molecular genetics · 2019Article
- Data set for transcriptional response to depletion of the Shoc2 scaffolding protein.Data in brief · 2016Article
- The function of Shoc2: A scaffold and beyond.Communicative & integrative biologyArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway plays a central role in defining various cellular fates. Scaffold proteins modulating ERK1/2 activity control growth factor signals transduced by the pathway. Here, we analyzed signals transduced by Shoc2, a critical positive modulator of ERK1/2 activity. We found that loss of Shoc2 results in impaired cell motility and delays cell attachment. As ERKs control cellular fates by stimulating transcriptional response, we hypothesized that the mechanisms underlying changes in cell adhesion could be revealed by assessing the changes in transcription of Shoc2-depleted cells. Using quantitative RNA-seq analysis, we identified 853 differentially expressed transcripts. Characterization of the differentially expressed genes showed that Shoc2 regulates the pathway at several levels, including expression of genes controlling cell motility, adhesion, crosstalk with the transforming growth factor beta (TGFβ) pathway, and expression of transcription factors. To understand the mechanisms underlying delayed attachment of cells depleted of Shoc2, changes in expression of the protein of extracellular matrix (lectin galactoside-binding soluble 3-binding protein; LGALS3BP) were functionally analyzed. We demonstrated that delayed adhesion of the Shoc2-depleted cells is a result of attenuated expression and secretion of LGALS3BP. Together our results suggest that Shoc2 regulates cell motility by modulating ERK1/2 signals to cell adhesion.
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Registered trials
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