ArticleThe Journal of biological chemistry2015
Phosphorylation of Serine 402 Regulates RacGAP Protein Activity of FilGAP Protein.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- FilGAP regulates tumor growth in Glioma through the regulation of mTORC1 and mTORC2.Scientific reports · 2023Article
- FilGAP, a GAP for Rac1, down-regulates invadopodia formation in breast cancer cells.Cell structure and function · 2023Article
- Spatiotemporal regulation of Rho GTPase signaling during endothelial barrier remodeling.Current opinion in physiology · 2023Review
- Durotaxis: the mechanical control of directed cell migration.The FEBS journal · 2022Review
- Connections between the cell cycle, cell adhesion and the cytoskeleton.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Rac activation is key to cell motility and directionality: An experimental and modelling investigation.Computational and structural biotechnology journal · 2019Article
- Validation of Osteogenic Properties of Cytochalasin D by High-Resolution RNA-Sequencing in Mesenchymal Stem Cells Derived from Bone Marrow and Adipose Tissues.Stem cells and development · 2018Article
- Myosin-dependent actin stabilization as revealed by single-molecule imaging of actin turnover.Molecular biology of the cell · 2018Article
- Roles of the novel coiled-coil protein Rng10 in septum formation during fission yeast cytokinesis.Molecular biology of the cell · 2016Article
- Regulating Rho GTPases and their regulators.Nature reviews. Molecular cell biology · 2016Review
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FilGAP is a Rho GTPase-activating protein (GAP) that specifically regulates Rac. FilGAP is phosphorylated by ROCK, and this phosphorylation stimulates its RacGAP activity. However, it is unclear how phosphorylation regulates cellular functions and localization of FilGAP. We found that non-phosphorylatable FilGAP (ST/A) mutant is predominantly localized to the cytoskeleton along actin filaments and partially co-localized with vinculin around cell periphery, whereas phosphomimetic FilGAP (ST/D) mutant is diffusely cytoplasmic. Moreover, phosphorylated FilGAP detected by Phos-tag is also mainly localized in the cytoplasm. Of the six potential phosphorylation sites in FilGAP tested, only mutation of serine 402 to alanine (S402A) resulted in decreased cell spreading on fibronectin. FilGAP phosphorylated at Ser-402 is localized to the cytoplasm but not at the cytoskeleton. Although Ser-402 is highly phosphorylated in serum-starved quiescent cells, dephosphorylation of Ser-402 is accompanied with the cell spreading on fibronectin. Treatment of the cells expressing wild-type FilGAP with calyculin A, a Ser/Thr phosphatase inhibitor, suppressed cell spreading on fibronectin, whereas cells transfected with FilGAP S402A mutant were not affected by calyculin A. Expression of constitutively activate Arf6 Q67L mutant stimulated membrane blebbing activity of both non-phosphorylatable (ST/A) and phosphomimetic (ST/D) FilGAP mutants. Conversely, depletion of endogenous Arf6 suppressed membrane blebbing induced by FilGAP (ST/A) and (ST/D) mutants. Our study suggests that Arf6 and phosphorylation of FilGAP may regulate FilGAP, and phosphorylation of Ser-402 may play a role in the regulation of cell spreading on fibronectin.
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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.