ArticleProstaglandins & other lipid mediators2008
Lack of a significant role of P-Rex1, a major regulator of macrophage Rac1 activation and chemotaxis, in atherogenesis.
Article in Prostaglandins & other lipid mediators, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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
15 citing papers in PubMed, 21 citations in OpenAlex.
- Inhibition of PREX1 Reverses Enzalutamide Resistance in Castration-Resistant Prostate Cancer.The world journal of men's health · 2026Article
- Review
- Identification of genes associated with smell dysfunction in Parkinson's disease.Clinical parkinsonism & related disorders · 2026Article
- P-Rex1 limits the agonist-induced internalization of GPCRs independently of its Rac-GEF activity.Cell reports · 2025Article
- Polymorphic tandem repeats influence cell type-specific gene expression across the human immune landscape.bioRxiv : the preprint server for biology · 2025Article
- P-Rex1 controls phagocytosis and the killing of bacteria by murine neutrophils independently of its catalytic activity.Frontiers in immunology · 2025Article
- Integrated Single-cell and Transcriptome Sequencing Analyses Identified PREX1 as an Immune-related Prognostic Biomarker for Liver Hepatocellular Carcinoma.International journal of medical sciences · 2024Article
- Article
- The GPCR adaptor protein norbin suppresses the neutrophil-mediated immunity of mice to pneumococcal infection.Blood advances · 2021Article
- The Emerging Role of Rho Guanine Nucleotide Exchange Factors in Cardiovascular Disorders: Insights Into Atherosclerosis: A Mini Review.Frontiers in cardiovascular medicine · 2021Review
- Phosphatidylinositol-3,4,5-trisphosphate dependent Rac exchange factor 1 is a diagnostic and prognostic biomarker for hepatocellular carcinoma.World journal of clinical cases · 2020Article
- Regulation and function of P-Rex family Rac-GEFs.Small GTPases · 2015Review
- A GEF-to-phospholipase molecular switch caused by phosphatidic acid, Rac and JAK tyrosine kinase that explains leukocyte cell migration.Journal of cell science · 2013Article
- Rac signaling in breast cancer: a tale of GEFs and GAPs.Cellular signalling · 2012Review
- Upregulation of PIP3-dependent Rac exchanger 1 (P-Rex1) promotes prostate cancer metastasis.Oncogene · 2009Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundRho GTPases are known to play important roles in regulating multiple cellular processes that include cell polarization and migration. Among these Rho GTPases, Rac has been shown to be essential for F actin formation and cell migration. P-Rex1 is a guanine nucleotide exchange factor (GEF) that was previously found to mediate the activation of Rac2, but not Rac1, in mouse neutrophils.
objectivesHere we examined the role of P-Rex1 in mouse macrophages and atherogenesis. METHODS AND
resultsPBD (p21 binding domain) pull down assay was performed to compare the Rac1 activation in WT and P-Rex1-deficient macrophage. In addition, transwell assay was conducted to compare chemotaxis of WT and P-Rex1-deficient macrophage. We found that P-Rex1 is a major Rac1 regulator in mouse macrophages as its deficiency significantly compromises macrophage chemotaxis, superoxide production (SOD), and Rac1 activation in response to chemoattractants. The potential role of P-Rex1 in atherogenesis is also investigated by transferring P-Rex1-deficient bone marrow cells to LDLR deficient mice. Contrary to our prediction, P-Rex1 deficiency did not alter atherogenesis, suggesting chemoattractant-induced macrophage migration may not have a significant role in atherogenesis.
conclusionsP-Rex1 is one of the major GEFs in macrophage regulating Rac1 activation and chemotaxis.
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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.