ArticleThe Journal of experimental medicine2014
The small GTPase Rap1b negatively regulates neutrophil chemotaxis and transcellular diapedesis by inhibiting Akt activation.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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Who cites it
28 citing papers in PubMed, 60 citations in OpenAlex.
- The Interplay between Integrins and Immune Cells as a Regulator in Cancer Immunology.International journal of molecular sciences · 2023Review
- Sex-Based Differences in Human Neutrophil Chemorepulsion.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Rap1b-loss increases neutrophil lactate dehydrogenase activity to enhance neutrophil migration and acute inflammationFrontiers in immunology · 2022Article
- Prognostic and immunological role of Ras-related protein Rap1b in pan-cancer.Bioengineered · 2021Article
- Suppressive Role of Bam32/DAPP1 in Chemokine-Induced Neutrophil Recruitment.International journal of molecular sciences · 2021Article
- The DNA Repair Enzyme XPD Is Partially Regulated by PI3K/AKT Signaling in the Context of Bupivacaine-Mediated Neuronal DNA Damage.Oxidative medicine and cellular longevity · 2021Article
- Saliva proteomic patterns in patients with molar incisor hypomineralization.Scientific reports · 2020Article
- Angiotensin-(1-7) Attenuates Protein O-GlcNAcylation in the Retina by EPAC/Rap1-Dependent Inhibition of O-GlcNAc Transferase.Investigative ophthalmology & visual science · 2020Article
- Review
- Staphylococcus aureus drives expansion of low-density neutrophils in diabetic mice.The Journal of clinical investigation · 2019Article
- Targeting allosteric site of AKT by 5,7-dimethoxy-1,4-phenanthrenequinone suppresses neutrophilic inflammation.EBioMedicine · 2019Article
- Metabolic Insight of Neutrophils in Health and Disease.Frontiers in immunology · 2019Review
- Two novel, putative mechanisms of action for citalopram-induced platelet inhibition.Scientific reports · 2018Article
- Human Plasmablast Migration Toward CXCL12 Requires Glucose Oxidation by Enhanced Pyruvate Dehydrogenase ActivityFrontiers in immunology · 2018Article
- Shp1 function in myeloid cells.Journal of leukocyte biology · 2017Review
- Rap1b Is an Effector of Axin2 Regulating Crosstalk of Signaling Pathways During Skeletal Development.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- Endothelial CD2AP Binds the Receptor ICAM-1 To Control Mechanosignaling, Leukocyte Adhesion, and the Route of Leukocyte Diapedesis In Vitro.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Acarbose Accelerates Wound Healing via Akt/eNOS Signaling inOxidative medicine and cellular longevity · 2017Article
- Manipulating the air-filled zebrafish swim bladder as a neutrophilic inflammation model for acute lung injury.Cell death & disease · 2016Article
- An Alternative Approach for Sample Preparation with Low Cell Number for TEM Analysis.Journal of visualized experiments : JoVE · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Neutrophils are the first line of cellular defense in response to infections and inflammatory injuries. However, neutrophil activation and accumulation into tissues trigger tissue damage due to release of a plethora of toxic oxidants and proteases, a cause of acute lung injury (ALI). Despite its clinical importance, the molecular regulation of neutrophil migration is poorly understood. The small GTPase Rap1b is generally viewed as a positive regulator of immune cell functions by controlling bidirectional integrin signaling. However, we found that Rap1b-deficient mice exhibited enhanced neutrophil recruitment to inflamed lungs and enhanced susceptibility to endotoxin shock. Unexpectedly, Rap1b deficiency promoted the transcellular route of diapedesis through endothelial cell. Increased transcellular migration of Rap1b-deficient neutrophils in vitro was selectively mediated by enhanced PI3K-Akt activation and invadopodia-like protrusions. Akt inhibition in vivo suppressed excessive Rap1b-deficient neutrophil migration and associated endotoxin shock. The inhibitory action of Rap1b on PI3K signaling may be mediated by activation of phosphatase SHP-1. Thus, this study reveals an unexpected role for Rap1b as a key suppressor of neutrophil migration and lung inflammation.
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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.