ArticleJournal of cell science2015
Front-signal-dependent accumulation of the RHOA inhibitor FAM65B at leading edges polarizes neutrophils.
Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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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
20 citing papers in PubMed, 26 citations in OpenAlex.
- RIPOR2 promotes multinucleation of melanoma cells downstream of the RAS/ERK oncogenic pathway.iScience · 2026Article
- Quantitative proteomics and phosphoproteomics reveal glucocorticoid stimulation of TLR and Rho GTPase signaling in neutrophil-like cells.Genome biology · 2026Article
- [Diagnostic efficacy of serum 14-3-3β protein combined with fractional exhaled nitric oxide and conventional ventilatory lung function parameters for bronchial asthma in children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Article
- Role of RHO family interacting cell polarization regulators (RIPORs) in health and disease: Recent advances and prospects.International journal of biological sciences · 2022Review
- RHO GTPases: from new partners to complex immune syndromes.Nature reviews. Immunology · 2021Review
- Monitoring Phosphoinositide Fluxes and Effectors During Leukocyte Chemotaxis and Phagocytosis.Frontiers in cell and developmental biology · 2021Review
- AJournal of medical genetics · 2020Article
- The circular RNA ACR attenuates myocardial ischemia/reperfusion injury by suppressing autophagy via modulation of the Pink1/ FAM65B pathway.Cell death and differentiation · 2019Article
- Leukocyte Cytoskeleton Polarization Is Initiated by Plasma Membrane Curvature from Cell Attachment.Developmental cell · 2019Article
- Revealing a human p53 universe.Nucleic acids research · 2018Article
- Fam65b Phosphorylation Relieves Tonic RhoA Inhibition During T Cell Migration.Frontiers in immunology · 2018Article
- Interaction between Rho GTPases and 14-3-3 Proteins.International journal of molecular sciences · 2017Review
- PKN1 Directs Polarized RAB21 Vesicle Trafficking via RPH3A and Is Important for Neutrophil Adhesion and Ischemia-Reperfusion Injury.Cell reports · 2017Article
- RHO binding to FAM65A regulates Golgi reorientation during cell migration.Journal of cell science · 2016Article
- Cancer derived peptide of vacuolar ATPase 'a2' isoform promotes neutrophil migration by autocrine secretion of IL-8.Scientific reports · 2016Article
- Article
- Article
- Effect of shRNA targeted against RhoA on proliferation and migration of human colonic cancer cells.International journal of clinical and experimental pathology · 2015Article
- Developmental regulation of planar cell polarity and hair-bundle morphogenesis in auditory hair cells: lessons from human and mouse genetics.Wiley interdisciplinary reviews. Developmental biologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
A hallmark of neutrophil polarization is the back localization of active RHOA and phosphorylated myosin light chain (pMLC, also known as MYL2). However, the mechanism for the polarization is not entirely clear. Here, we show that FAM65B, a newly identified RHOA inhibitor, is important for the polarization. When FAM65B is phosphorylated, it binds to 14-3-3 family proteins and becomes more stable. In neutrophils, chemoattractants stimulate FAM65B phosphorylation largely depending on the signals from the front of the cells that include those mediated by phospholipase Cβ (PLCβ) and phosphoinositide 3-kinase γ (PI3Kγ), leading to FAM65B accumulation at the leading edge. Concordantly, FAM65B deficiency in neutrophils resulted in an increase in RHOA activity and localization of pMLC to the front of cells, as well as defects in chemotaxis directionality and adhesion to endothelial cells under flow. These data together elucidate a mechanism for RHOA and pMLC polarization in stimulated neutrophils through direct inhibition of RHOA by FAM65B at the leading edge.
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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.