ArticleAmerican journal of physiology. Renal physiology2014
Exocyst Sec10 protects renal tubule cells from injury by EGFR/MAPK activation and effects on endocytosis.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Deletion of exocyst component 5 suppresses repair of injured kidney by limiting cell proliferation.Cell death discovery · 2026Article
- Deficiency of exocyst complex component Exoc5 exacerbates the progression of kidney fibrosis.Experimental & molecular medicine · 2026Article
- The exocyst in ciliogenesis.Renal failure · 2025Review
- Sec10 suppresses antiviral innate immune response by facilitating STUB1-mediated STAT1 degradation.PLoS pathogens · 2025Article
- Targeting the epidermal growth factor receptor (EGFR/ErbB) for the potential treatment of renal pathologies.Frontiers in pharmacology · 2024Review
- Regulation of EGF-stimulated activation of the PI-3K/AKT pathway by exocyst-mediated exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Primary cilia and the exocyst are linked to urinary extracellular vesicle production and content.The Journal of biological chemistry · 2019Article
- The role of the exocyst in renal ciliogenesis, cystogenesis, tubulogenesis, and development.Kidney research and clinical practice · 2019Review
- The exocyst functions in niche cells to promote germline stem cell differentiation by directly controlling EGFR membrane trafficking.Development (Cambridge, England) · 2019Article
- The exocyst acting through the primary cilium is necessary for renal ciliogenesis, cystogenesis, and tubulogenesis.The Journal of biological chemistry · 2019Article
- Roles for IFT172 and Primary Cilia in Cell Migration, Cell Division, and Neocortex Development.Frontiers in cell and developmental biology · 2019Article
- Regulation of Cell Polarity by Exocyst-Mediated Trafficking.Cold Spring Harbor perspectives in biology · 2018Review
- Neutral Competition forGenetics · 2017Article
- Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury.Journal of visualized experiments : JoVE · 2016Article
- Insights into kidney stem cell development and regeneration using zebrafish.World journal of stem cells · 2016Review
- The Exocyst Complex in Health and Disease.Frontiers in cell and developmental biology · 2016Review
- Zebrafish Renal Pathology: Emerging Models of Acute Kidney Injury.Current pathobiology reportsReview
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Acute kidney injury is common and has a high mortality rate, and no effective treatment exists other than supportive care. Using cell culture models, we previously demonstrated that exocyst Sec10 overexpression reduced damage to renal tubule cells and speeded recovery and that the protective effect was mediated by higher basal levels of mitogen-activated protein kinase (MAPK) signaling. The exocyst, a highly-conserved eight-protein complex, is known for regulating protein trafficking. Here we show that the exocyst biochemically interacts with the epidermal growth factor receptor (EGFR), which is upstream of MAPK, and Sec10-overexpressing cells express greater levels of phosphorylated (active) ERK, the final step in the MAPK pathway, in response to EGF stimulation. EGFR endocytosis, which has been linked to activation of the MAPK pathway, increases in Sec10-overexpressing cells, and gefitinib, a specific EGFR inhibitor, and Dynasore, a dynamin inhibitor, both reduce EGFR endocytosis. In turn, inhibition of the MAPK pathway reduces ligand-mediated EGFR endocytosis, suggesting a potential feedback of elevated ERK activity on EGFR endocytosis. Gefitinib also decreases MAPK signaling in Sec10-overexpressing cells to levels seen in control cells and, demonstrating a causal role for EGFR, reverses the protective effect of Sec10 overexpression following cell injury in vitro. Finally, using an in vivo zebrafish model of acute kidney injury, morpholino-induced knockdown of sec10 increases renal tubule cell susceptibility to injury. Taken together, these results suggest that the exocyst, acting through EGFR, endocytosis, and the MAPK pathway is a candidate therapeutic target for acute kidney injury.
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