ArticleGenes & development2018
Merlin/ERM proteins regulate growth factor-induced macropinocytosis and receptor recycling by organizing the plasma membrane:cytoskeleton interface.
Article in Genes & development, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Metabolic vulnerabilities in pleural mesothelioma.Oncogenesis · 2026Review
- NF2 loss malignantly transforms human pancreatic acinar cells and enhances cell fitness under environmental stress.The Journal of clinical investigation · 2026Article
- Interactions among Merlin, Arkadia, and SKOR2 mediate NF2-associated human Schwann cell proliferation.Stem cell research & therapy · 2025Article
- NF2: An underestimated player in cancer metabolic reprogramming and tumor immunity.NPJ precision oncology · 2024Review
- Mechanical stretch regulates macropinocytosis inMolecular biology of the cell · 2024Article
- Hippo Signaling Pathway in Colorectal Cancer: Modulation by Various Signals and Therapeutic Potential.Analytical cellular pathology (Amsterdam) · 2024Review
- Cellular mechanisms of heterogeneity in NF2-mutant schwannoma.Nature communications · 2023Article
- Cadherins and catenins in cancer: connecting cancer pathways and tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- Antisense oligonucleotides targeting exon 11 are able to partially rescue the NF2-related schwannomatosis phenotypeMolecular therapy. Nucleic acids · 2022Article
- Complexity of progranulin mechanisms of action in mesothelioma.Journal of experimental & clinical cancer research : CR · 2022Article
- Gene replacement therapy in a schwannoma mouse model of neurofibromatosis type 2.Molecular therapy. Methods & clinical development · 2022Article
- Review
- Circular dorsal ruffles disturb the growth factor-induced PI3K-AKT pathway in hepatocellular carcinoma Hep3B cells.Cell communication and signaling : CCS · 2022Article
- Signaling Pathways that Regulate Macropinocytosis in Mammalian Cells.Sub-cellular biochemistry · 2022Article
- The Role and Therapeutic Potential of Macropinocytosis in Cancer.Frontiers in pharmacology · 2022Review
- Osimertinib-resistant NSCLC cells activate ERBB2 and YAP/TAZ and are killed by neratinib.Biochemical pharmacology · 2021Article
- The GAS6-AXL signaling pathway triggers actin remodeling that drives membrane ruffling, macropinocytosis, and cancer-cell invasion.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Wnt/β-catenin signaling: Structure, assembly and endocytosis of the signalosome.Development, growth & differentiation · 2021Review
- A potent and selective small molecule inhibitor of myoferlin attenuates colorectal cancer progression.Clinical and translational medicine · 2021Article
- From Pinocytosis to Methuosis-Fluid Consumption as a Risk Factor for Cell Death.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The architectural and biochemical features of the plasma membrane are governed by its intimate association with the underlying cortical cytoskeleton. The neurofibromatosis type 2 (NF2) tumor suppressor merlin and closely related membrane:cytoskeleton-linking protein ezrin organize the membrane:cytoskeleton interface, a critical cellular compartment that both regulates and is regulated by growth factor receptors. An example of this poorly understood interrelationship is macropinocytosis, an ancient process of nutrient uptake and membrane remodeling that can both be triggered by growth factors and manage receptor availability. We show that merlin deficiency primes the membrane:cytoskeleton interface for epidermal growth factor (EGF)-induced macropinocytosis via a mechanism involving increased cortical ezrin, altered actomyosin, and stabilized cholesterol-rich membranes. These changes profoundly alter EGF receptor (EGFR) trafficking in merlin-deficient cells, favoring increased membrane levels of its heterodimerization partner, ErbB2; clathrin-independent internalization; and recycling. Our work suggests that, unlike Ras transformed cells, merlin-deficient cells do not depend on macropinocytic protein scavenging and instead exploit macropinocytosis for receptor recycling. Finally, we provide evidence that the macropinocytic proficiency of NF2-deficient cells can be used for therapeutic uptake. This work provides new insight into fundamental mechanisms of macropinocytic uptake and processing and suggests new ways to interfere with or exploit macropinocytosis in
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