ArticleBlood2015
P-Rex and Vav Rac-GEFs in platelets control leukocyte recruitment to sites of inflammation.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
The trial behind it
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
39 citing papers in PubMed, 87 citations in OpenAlex.
- Platelet-specific P2YRespiratory research · 2026Article
- Immune-inflammation markers are related to hormone levels in polycystic ovary syndrome: a case-control study : Immune-inflammatory markers in PCOS.BMC endocrine disorders · 2025Article
- P-Rex1 limits the agonist-induced internalization of GPCRs independently of its Rac-GEF activity.Cell reports · 2025Article
- Pseudomonas aeruginosa infection exacerbates elastase induced lung damage: characterisation of a novel murine two-hit model of pulmonary infection.Respiratory research · 2025Article
- P-Rex1 controls phagocytosis and the killing of bacteria by murine neutrophils independently of its catalytic activity.Frontiers in immunology · 2025Article
- Vav family exchange factors: Potential regulator in atherosclerosis.Biochemistry and biophysics reports · 2024Review
- Stimulation of platelet P2YBritish journal of pharmacology · 2024Article
- Exploring bias in platelet P2YBritish journal of pharmacology · 2024Review
- Advances in immune response to pulmonary infection: Nonspecificity, specificity and memory.Chronic diseases and translational medicine · 2023Review
- Dock2 generates characteristic spatiotemporal patterns of Rac activity to regulate neutrophil polarisation, migration and phagocytosis.Frontiers in immunology · 2023Article
- The Rac-GEF Tiam1 controls integrin-dependent neutrophil responses.Frontiers in immunology · 2023Article
- Platelet-leukocyte crosstalk in COVID-19: How might the reciprocal links between thrombotic events and inflammatory state affect treatment strategies and disease prognosis?Thrombosis research · 2022Review
- Heparin-Functionalized Adsorbents Eliminate Central Effectors of Immunothrombosis, including Platelet Factor 4, High-Mobility Group Box 1 Protein and Histones.International journal of molecular sciences · 2022Article
- RNA Sequencing Reveals the Regulation Mechanism of Yunnan Baiyao in Treating Skin Infection Caused byEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Activated Platelets and Platelet-Derived Extracellular Vesicles Mediate COVID-19-Associated Immunothrombosis.Frontiers in cell and developmental biology · 2022Review
- Small-molecule inhibitors of P-Rex guanine-nucleotide exchange factors.Small GTPases · 2022Article
- Article
- The GPCR adaptor protein norbin suppresses the neutrophil-mediated immunity of mice to pneumococcal infection.Blood advances · 2021Article
- Platelet Innate Immune Receptors and TLRs: A Double-Edged Sword.International journal of molecular sciences · 2021Review
- Platelets Independently Recruit into Asthmatic Lungs and Models of Allergic Inflammation via CCR3.American journal of respiratory cell and molecular biology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The small GTPase Rac is required for neutrophil recruitment during inflammation, but its guanine-nucleotide exchange factor (GEF) activators seem dispensable for this process, which led us to investigate the possibility of cooperation between Rac-GEF families. Thioglycollate-induced neutrophil recruitment into the peritoneum was more severely impaired in P-Rex1(-/-) Vav1(-/-) (P1V1) or P-Rex1(-/-) Vav3(-/-) (P1V3) mice than in P-Rex null or Vav null mice, suggesting cooperation between P-Rex and Vav Rac-GEFs in this process. Neutrophil transmigration and airway infiltration were all but lost in P1V1 and P1V3 mice during lipopolysaccharide (LPS)-induced pulmonary inflammation, with altered intercellular adhesion molecule 1-dependent slow neutrophil rolling and strongly reduced L- and E-selectin-dependent adhesion in airway postcapillary venules. Analysis of adhesion molecule expression, neutrophil adhesion, spreading, and migration suggested that these defects were only partially neutrophil-intrinsic and were not obviously involving vascular endothelial cells. Instead, P1V1 and P1V3 platelets recapitulated the impairment of LPS-induced intravascular neutrophil adhesion and recruitment, showing P-Rex and Vav expression in platelets to be crucial. Similarly, during ovalbumin-induced allergic inflammation, pulmonary recruitment of P1V1 and P1V3 eosinophils, monocytes, and lymphocytes was compromised in a platelet-dependent manner, and airway inflammation was essentially abolished, resulting in improved airway responsiveness. Therefore, platelet P-Rex and Vav family Rac-GEFs play important proinflammatory roles in leukocyte recruitment.
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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.