ArticleJournal of cellular and molecular medicine2011
Regulation of dynamin-2 assembly-disassembly and function through the SH3A domain of intersectin-1s.
Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Intersectin1 promotes clathrin-mediated endocytosis by organizing and stabilizing endocytic protein interaction networks.Cell reports · 2024Article
- Dysregulation of the Long Noncoding RNA X-Inactive-Specific Transcript Expression in Male Patients with Pulmonary Arterial Hypertension.The American journal of pathology · 2024Article
- Intersectin1 promotes clathrin-mediated endocytosis by organizing and stabilizing endocytic protein interaction networks.bioRxiv : the preprint server for biology · 2024Article
- Dynole 34-2 and Acrylo-Dyn 2-30, Novel Dynamin GTPase Chemical Biology Probes.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Sex differences in the proliferation of pulmonary artery endothelial cells: implications for plexiform arteriopathy.Journal of cell science · 2020Article
- Lung Endothelial Transcytosis.Comprehensive Physiology · 2020Review
- Tks5 and Dynamin-2 enhance actin bundle rigidity in invadosomes to promote myoblast fusion.The Journal of cell biology · 2019Article
- Epsin15 Homology Domains: Role in the Pathogenesis of Pulmonary Arterial Hypertension.Frontiers in physiology · 2018Article
- Intersectin-1s deficiency in pulmonary pathogenesis.Respiratory research · 2017Review
- Endocytic deficiency induced by ITSN-1s knockdown alters the Smad2/3-Erk1/2 signaling balance downstream of Alk5.Journal of cell science · 2015Article
- SH3 Domains Differentially Stimulate Distinct Dynamin I Assembly Modes and G Domain Activity.PloS one · 2015Article
- Building a better dynasore: the dyngo compounds potently inhibit dynamin and endocytosis.Traffic (Copenhagen, Denmark) · 2013Article
- A novel p38 mitogen-activated protein kinase/Elk-1 transcription factor-dependent molecular mechanism underlying abnormal endothelial cell proliferation in plexogenic pulmonary arterial hypertension.The Journal of biological chemistry · 2013Article
- Intersectin-1s: an important regulator of cellular and molecular pathways in lung injury.Pulmonary circulation · 2013Article
- Emerging roles for intersectin (ITSN) in regulating signaling and disease pathways.International journal of molecular sciences · 2013Review
- In vivo knockdown of intersectin-1s alters endothelial cell phenotype and causes microvascular remodeling in the mouse lungs.Apoptosis : an international journal on programmed cell death · 2013Article
- Impaired caveolae function and upregulation of alternative endocytic pathways induced by experimental modulation of intersectin-1s expression in mouse lung endothelium.Biochemistry research international · 2012Article
- Pro-inflammatory endothelial cell dysfunction is associated with intersectin-1s down-regulation.Respiratory research · 2011Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Intersectin-1s (ITSN-1s), a five Src homology 3 (SH3) domain-containing protein, is critically required for caveolae and clathrin-mediated endocytosis (CME), due to its interactions with dynamin (dyn). Of the five SH3A-E domains, SH3A is unique because of its high affinity for dyn and potent inhibition of CME. However, the molecular mechanism by which SH3A integrates in the overall function of ITSN-1s to regulate the endocytic process is not understood. Using biochemical and functional approaches as well as high-resolution electron microscopy, we show that SH3A exogenously expressed in human lung endothelial cells caused abnormal endocytic structures, distorted caveolae clusters, frequent staining-dense rings around the caveolar necks and 60% inhibition of caveolae internalization. In vitro studies further revealed that SH3A, similar to full-length ITSN-1s stimulates dyn2 oligomerization and guanosine triphosphatase (GTP)ase activity, effects not detected when other SH3 domains of ITSN-1s were used as controls. Strikingly, in the presence of SH3A, dyn2-dyn2 interactions are stabilized and despite continuous GTP hydrolysis, dyn2 oligomers cannot disassemble. SH3A may hold up caveolae release from the plasma membrane and formation of free-transport vesicles, by prolonging the lifetime of assembled dyn2. Altogether, our results indicate that ITSN-1s, via its SH3A has the unique ability to regulate dyn2 assembly-disassembly and function during endocytosis.
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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.