ArticleMolecular biology of the cell2012
Cell surface annexins regulate ADAM-mediated ectodomain shedding of proamphiregulin.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- The Therapeutic Potential of ADAMTS8 in Lung Adenocarcinoma without Targetable Therapy.Journal of personalized medicine · 2022Article
- ADAM-10 Regulates MMP-12 during Lipopolysaccharide-Induced Inflammatory Response in Macrophages.Journal of immunology research · 2022Article
- HPV16 Entry into Epithelial Cells: Running a Gauntlet.Viruses · 2021Review
- NADPH Oxidase and Epidermal Growth Factor Receptor Are Promising Targets of Phytochemicals for Ultraviolet-Induced Skin Carcinogenesis.Antioxidants (Basel, Switzerland) · 2021Review
- The long and winding road: human papillomavirus entry and subcellular trafficking.Current opinion in virology · 2021Review
- Functional Genomics Approach Identifies Novel Signaling Regulators of TGFα Ectodomain Shedding.Molecular cancer research : MCR · 2018Article
- ADAM and ADAMTS Family Proteins and Snake Venom Metalloproteinases: A Structural Overview.Toxins · 2016Review
- Ectodomain Shedding of Lymphatic Vessel Endothelial Hyaluronan Receptor 1 (LYVE-1) Is Induced by Vascular Endothelial Growth Factor A (VEGF-A).The Journal of biological chemistry · 2016Article
- CD147 regulates cancer migration via direct interaction with Annexin A2 and DOCK3-β-catenin-WAVE2 signaling.Oncotarget · 2016Article
- Reversible interconversion and maintenance of mammary epithelial cell characteristics by the ligand-regulated EGFR system.Scientific reports · 2016Article
- Distinct Intracellular Domain Substrate Modifications Selectively Regulate Ectodomain Cleavage of NRG1 or CD44.Molecular and cellular biology · 2015Article
- Advances in refractory ulcerative colitis treatment: A new therapeutic target, Annexin A2.World journal of gastroenterology · 2015Review
- Inside-out Regulation of Ectodomain Cleavage of Cluster-of-Differentiation-44 (CD44) and of Neuregulin-1 Requires Substrate Dimerization.The Journal of biological chemistry · 2015Article
- Characterization and mechanism of stress-induced translocation of 78-kilodalton glucose-regulated protein (GRP78) to the cell surface.The Journal of biological chemistry · 2015Article
- Article
- Differential expression and localization of ADAM10 and ADAM17 during rat spermatogenesis suggest a role in germ cell differentiation.Biological research · 2014Article
- Bioinformatics analysis of bacterial annexins--putative ancestral relatives of eukaryotic annexins.PloS one · 2014Article
- A mechanism of male germ cell apoptosis induced by bisphenol-A and nonylphenol involving ADAM17 and p38 MAPK activation.PloS one · 2014Article
- Annexin A2 and S100A10 regulate human papillomavirus type 16 entry and intracellular trafficking in human keratinocytes.Journal of virology · 2013Article
- Human antigen R-mediated mRNA stabilization is required for ultraviolet B-induced autoinduction of amphiregulin in keratinocytes.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A disintegrin and metalloproteinase (ADAM) is a family of enzymes involved in ectodomain shedding of various membrane proteins. However, the molecular mechanism underlying substrate recognition by ADAMs remains unknown. In this study, we successfully captured and analyzed cell surface transient assemblies between the transmembrane amphiregulin precursor (proAREG) and ADAM17 during an early shedding phase, which enabled the identification of cell surface annexins as components of their shedding complex. Annexin family members annexin A2 (ANXA2), A8, and A9 interacted with proAREG and ADAM17 on the cell surface. Shedding of proAREG was increased when ANXA2 was knocked down but decreased with ANXA8 and A9 knockdown, because of enhanced and impaired association with ADAM17, respectively. Knockdown of ANXA2 and A8 in primary keratinocytes altered wound-induced cell migration and ultraviolet B-induced phosphorylation of epidermal growth factor receptor (EGFR), suggesting that annexins play an essential role in the ADAM-mediated ectodomain shedding of EGFR ligands. On the basis of these data, we propose that annexins on the cell surface function as "shedding platform" proteins to determine the substrate selectivity of ADAM17, with possible therapeutic potential in ADAM-related diseases.
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