ArticlePloS one2012
Shoc2 is targeted to late endosomes and required for Erk1/2 activation in EGF-stimulated cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- The expression of congenital Shoc2 variants induces AKT-dependent crosstalk activation of the ERK1/2 pathway.Human molecular genetics · 2024Article
- A Leucine-Rich Repeat Protein Provides a SHOC2 the RAS Circuit: a Structure-Function Perspective.Molecular and cellular biology · 2021Review
- 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
- VCP/p97 controls signals of the ERK1/2 pathway transmitted via the Shoc2 scaffolding complex: novel insights into IBMPFD pathology.Molecular biology of the cell · 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
- Shoc2-tranduced ERK1/2 motility signals--Novel insights from functional genomics.Cellular signalling · 2016Article
- Unconventional EGF-induced ERK1/2-mediated Kv1.3 endocytosis.Cellular and molecular life sciences : CMLS · 2016Article
- Spatial control of Shoc2-scaffold-mediated ERK1/2 signaling requires remodeling activity of the ATPase PSMC5.Journal of cell science · 2015Article
- Research Resource: Androgen Receptor Activity Is Regulated Through the Mobilization of Cell Surface Receptor Networks.Molecular endocrinology (Baltimore, Md.) · 2015Article
- A Novel SHOC2 Variant in Rasopathy.Human mutation · 2014Article
- HUWE1 is a molecular link controlling RAF-1 activity supported by the Shoc2 scaffold.Molecular and cellular biology · 2014Article
- Shoc2/Sur8 protein regulates neurite outgrowth.PloS one · 2014Article
- The neuropilin 1 cytoplasmic domain is required for VEGF-A-dependent arteriogenesis.Developmental cell · 2013Article
- Desmoglein-1/Erbin interaction suppresses ERK activation to support epidermal differentiation.The Journal of clinical investigation · 2013Article
- Genetic basis of the impaired renal myogenic response in FHH rats.American journal of physiology. Renal physiology · 2013Article
- Article
- Spatial regulation of epidermal growth factor receptor signaling by endocytosis.International journal of molecular sciences · 2012Review
- The function of Shoc2: A scaffold and beyond.Communicative & integrative biologyArticle
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Shoc2 is the putative scaffold protein that interacts with RAS and RAF, and positively regulates signaling to extracellular signal-regulated protein kinases 1 and 2 (ERK1/2). To elucidate the mechanism by which Shoc2 regulates ERK1/2 activation by the epidermal growth factor (EGF) receptor (EGFR), we studied subcellular localization of Shoc2. Upon EGFR activation, endogenous Shoc2 and red fluorescent protein tagged Shoc2 were translocated from the cytosol to a subset of late endosomes containing Rab7. The endosomal recruitment of Shoc2 was blocked by overexpression of a GDP-bound H-RAS (N17S) mutant and RNAi knockdown of clathrin, suggesting the requirement of RAS activity and clathrin-dependent endocytosis. RNAi depletion of Shoc2 strongly inhibited activation of ERK1/2 by low, physiological EGF concentrations, which was rescued by expression of wild-type recombinant Shoc2. In contrast, the Shoc2 (S2G) mutant, that is myristoylated and found in patients with the Noonan-like syndrome, did not rescue ERK1/2 activation in Shoc2-depleted cells. Shoc2 (S2G) was not located in late endosomes but was present on the plasma membrane and early endosomes. These data suggest that targeting of Shoc2 to late endosomes may facilitate EGFR-induced ERK activation under physiological conditions of cell stimulation by EGF, and therefore, may be involved in the spatiotemporal regulation of signaling through the RAS-RAF module.
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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.