ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2012
Paxillin contracts the osteoclast cytoskeleton.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Paxillin mediates ARP2-dependent actin assembly for spindle migration in mammalian oocyte meiosis.Biology direct · 2026Article
- Paxillin and Kindlin: Research Progress and Biological Functions.Biomolecules · 2025Review
- Pulmonary osteoclast-like cells in silica induced pulmonary fibrosis.Science advances · 2024Article
- Modulation of the pre-metastatic bone niche: molecular changes mediated by bone-homing prostate cancer extracellular vesicles.Frontiers in cell and developmental biology · 2024Article
- Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis.Nature communications · 2023Article
- Pulmonary osteoclast-like cells in silica induced pulmonary fibrosis.bioRxiv : the preprint server for biology · 2023Article
- Distinct Concentration-Dependent Molecular Pathways Regulate Bone Cell Responses to Cobalt and Chromium Exposure from Joint Replacement Prostheses.International journal of molecular sciences · 2021Article
- The tethering function of mitofusin2 controls osteoclast differentiation by modulating the CaThe Journal of biological chemistry · 2020Article
- Myosins in Osteoclast Formation and Function.Biomolecules · 2018Review
- PGC1β Organizes the Osteoclast Cytoskeleton by Mitochondrial Biogenesis and Activation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
- Roles of paxillin family members in adhesion and ECM degradation coupling at invadosomes.The Journal of cell biology · 2016Article
- Osteoclasts-Key Players in Skeletal Health and Disease.Microbiology spectrum · 2016Review
- Alternative NF-κB Regulates RANKL-Induced Osteoclast Differentiation and Mitochondrial Biogenesis via Independent Mechanisms.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
- Phosphorylation of paxillin confers cisplatin resistance in non-small cell lung cancer via activating ERK-mediated Bcl-2 expression.Oncogene · 2014Article
- Vinculin regulates osteoclast function.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Osteoclastic bone resorption depends upon the cell's ability to organize its cytoskeleton via the αvβ3 integrin and osteoclastogenic cytokines. Because paxillin associates with αvβ3, we asked if it participates in skeletal degradation. Unlike deletion of other αvβ3-associated cytoskeleton-regulating molecules, which impairs the cell's ability to spread, paxillin-deficient (Pax(-/-) ) osteoclasts, generated from embryonic stem cells, "superspread" in response to receptor activator of NF-κB ligand (RANKL) and form large, albeit dynamically atypical, actin bands. Despite their increased size, Pax(-/-) osteoclasts resorb bone poorly, excavating pits approximately one-third normal depth. Ligand-occupied αvβ3 or RANKL promotes paxillin serine and tyrosine phosphorylation, the latter via cellular sarcoma (c-Src). The abnormal Pax(-/-) phenotype is rescued by wild-type (WT) paxillin but not that lacking its LD4 domain. In keeping with the appearance of mutant osteoclasts, WT paxillin, overexpressed in WT cells, contracts the cytoskeleton. Most importantly, the abnormal phenotype of Pax(-/-) osteoclasts likely represents failed RANKL-mediated delivery of myosin IIA to the actin cytoskeleton via the paxillin LD4 domain but is independent of tyrosine phosphorylation. Thus, in response to RANKL, paxillin associates with myosin IIA to contract the osteoclast cytoskeleton, thereby promoting its bone-degrading capacity.
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