ArticleProceedings of the National Academy of Sciences of the United States of America2005
Arp2/3 complex-deficient mouse fibroblasts are viable and have normal leading-edge actin structure and function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
- Arp2/3 complex activity is necessary for mouse ESC differentiation, times formative pluripotency, and enables lineage specification.Stem cell reports · 2022Article
- MICAL2 enhances branched actin network disassembly by oxidizing Arp3B-containing Arp2/3 complexes.The Journal of cell biology · 2021Article
- Induced Arp2/3 Complex Depletion Increases FMNL2/3 Formin Expression and Filopodia Formation.Frontiers in cell and developmental biology · 2021Article
- Division of Labor Between Two Actin Nucleators-the Formin FH1 and the ARP2/3 Complex-inFrontiers in plant science · 2020Article
- New insights into the formation and the function of lamellipodia and ruffles in mesenchymal cell migration.Cell adhesion & migration · 2018Review
- Nano-scale actin-network characterization of fibroblast cells lacking functional Arp2/3 complex.Journal of structural biology · 2017Article
- Advances and Future Directions for Tuberous Sclerosis Complex Research: Recommendations From the 2015 Strategic Planning Conference.Pediatric neurology · 2016Article
- Rice TUTOU1 Encodes a Suppressor of cAMP Receptor-Like Protein That Is Important for Actin Organization and Panicle Development.Plant physiology · 2015Article
- A mechanism of leading-edge protrusion in the absence of Arp2/3 complex.Molecular biology of the cell · 2015Article
- The Nck-interacting kinase NIK increases Arp2/3 complex activity by phosphorylating the Arp2 subunit.The Journal of cell biology · 2015Article
- Self-organization of protrusions and polarity during eukaryotic chemotaxis.Current opinion in cell biology · 2014Review
- The role of Arp2/3 in growth cone actin dynamics and guidance is substrate dependent.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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- FHOD1 is needed for directed forces and adhesion maturation during cell spreading and migration.Developmental cell · 2013Article
- Arp2/3 complex inhibitors adversely affect actin cytoskeleton remodeling in the cultured murine kidney collecting duct M-1 cells.Cell and tissue research · 2013Article
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- Investigating the role of the actin regulating complex ARP2/3 in rapid ischemic tolerance induced neuro-protection.International journal of physiology, pathophysiology and pharmacology · 2013Article
- Gadkin negatively regulates cell spreading and motility via sequestration of the actin-nucleating ARP2/3 complex.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- The Arp2/3 complex is required for lamellipodia extension and directional fibroblast cell migration.The Journal of cell biology · 2012Article
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA interference silencing of up to 90% of Arp3 protein expression, a major subunit of the Arp2/3 complex, proportionately decreases the intracellular motility of Listeria monocytogenes and actin nucleation activity ascribable to the Arp2/3 complex in mouse embryonic fibroblasts. However, the Arp2/3-deficient cells exhibit unimpaired lamellipodial actin network structure, translational locomotion, spreading, actin assembly, and ruffling responses. In addition, Arp3-silenced cells expressing neural Wiskott-Aldrich syndrome protein-derived peptides that inhibit Arp2/3 complex function in wild-type cells retained normal PDGF-induced ruffling. The Arp2/3 complex can be dispensable for leading-edge actin remodeling.
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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.