ArticleMolecular and cellular biology2011
The Aarskog-Scott syndrome protein Fgd1 regulates podosome formation and extracellular matrix remodeling in transforming growth factor β-stimulated aortic endothelial cells.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Cdc42 couples septin recruitment to the axial landmark assembly via Axl2 in budding yeast.Journal of cell science · 2024Article
- ARHGAP17 regulates the spatiotemporal activity of Cdc42 at invadopodia.The Journal of cell biology · 2023Article
- Super-resolution microscopy reveals nanoscale architecture and regulation of podosome clusters in primary macrophages.iScience · 2022Article
- Case Report: Aarskog-scott syndrome caused by FGD1 gene variation: A family study.Frontiers in genetics · 2022Article
- Intersection of TKS5 and FGD1/CDC42 signaling cascades directs the formation of invadopodia.The Journal of cell biology · 2020Article
- Multiple Rap1 effectors control Epac1-mediated tightening of endothelial junctions.Small GTPases · 2020Article
- Cortactin function in invadopodia.Small GTPases · 2020Review
- A proximity-labeling proteomic approach to investigate invadopodia molecular landscape in breast cancer cells.Scientific reports · 2020Article
- FGD1 promotes tumor progression and regulates tumor immune response in osteosarcoma via inhibiting PTEN activity.Theranostics · 2020Article
- Article
- High Expression of FGD3, a Putative Regulator of Cell Morphology and Motility, Is Prognostic of Favorable Outcome in Multiple Cancers.JCO precision oncology · 2017Article
- A network of conserved formins, regulated by the guanine exchange factor EXC-5 and the GTPase CDC-42, modulates tubulogenesis in vivo.Development (Cambridge, England) · 2016Article
- Computational Analysis of the Binding Specificities of PH Domains.BioMed research international · 2015Article
- ALK5 and ALK1 play antagonistic roles in transforming growth factor β-induced podosome formation in aortic endothelial cells.Molecular and cellular biology · 2014Article
- Bud3 activates Cdc42 to establish a proper growth site in budding yeast.The Journal of cell biology · 2014Article
- Src-dependent Tks5 phosphorylation regulates invadopodia-associated invasion in prostate cancer cells.The Prostate · 2014Article
- Rho GAPs and GEFs: controling switches in endothelial cell adhesion.Cell adhesion & migration · 2014Review
- Importance of RhoGTPases in formation, characteristics, and functions of invadosomes.Small GTPases · 2014Review
- Cdc42 and Tks5: a minimal and universal molecular signature for functional invadosomes.Cell adhesion & migration · 2014Article
- Spatiotemporal organization and mechanosensory function of podosomes.Cell adhesion & migration · 2014Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podosomes are dynamic actin-rich adhesion plasma membrane microdomains endowed with extracellular matrix-degrading activities. In aortic endothelial cells, podosomes are induced by transforming growth factor β (TGF-β), but how this occurs is largely unknown. It is thought that, in endothelial cells, podosomes play a role in vessel remodeling and/or in breaching anatomical barriers. We demonstrate here that, in bovine aortic endothelial cells, that the Cdc42-specific guanine exchange factor (GEF) Fgd1 is expressed and regulated by TGF-β to induce Cdc42-dependent podosome assembly. Within 15 min of TGF-β stimulation, Fgd1, but none of the other tested Cdc42 GEFs, undergoes tyrosine phosphorylation, associates with Cdc42, and translocates to the subcortical cytoskeleton via a cortactin-dependent mechanism. Small interfering RNA-mediated Fgd1 knockdown inhibits TGF-β-induced Cdc42 activation. Fgd1 depletion also reduces podosome formation and associated matrix degradation and these defects are rescued by reexpression of Fgd1. Although overexpression of Fgd1 does not promote podosome formation per se, it enhances TGF-β-induced matrix degradation. Our results identify Fgd1 as a TGF-β-regulated GEF and, as such, the first GEF to be involved in the process of cytokine-induced podosome formation. Our findings reveal the involvement of Fgd1 in endothelial cell biology and open up new avenues to study its role in vascular pathophysiology.
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