ArticleThe EMBO journal2012
GPCR activation of Ras and PI3Kc in neutrophils depends on PLCb2/b3 and the RasGEF RasGRP4.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 78 citations in OpenAlex.
- RASGRP4 is a key factor in the KRAS activation mediated by SOS in tumor Y1 adrenocortical cell lines.Scientific reports · 2026Article
- Article
- The CXCL8-CXCR2 axis promotes M2 macrophage polarization in ovarian cancer via RASGRP4-mediated mTOR-STAT3 signaling.Apoptosis : an international journal on programmed cell death · 2025Article
- RasGRP4 Exacerbates Diabetic Kidney Fibrosis via Aloxe3-Mediated Oxidative Stress and Scar-Associated Macrophage Activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Phospholipase C Beta 2 as a Key Regulator of Tumor Progression and Epithelial-Mesenchymal Transition via PI3K/AKT Signaling in Renal Cell Carcinoma.Biomedicines · 2025Article
- PLCγ2 controls neutrophil-like cell sensitivity through calcium oscillation and gates chemoattractant concentration range for chemotaxis.Frontiers in immunology · 2025Article
- Tear-derived extracellular vesicles as diagnostic biomarkers for ocular and neurodegenerative diseases: opportunities and challenges.Extracellular vesicles and circulating nucleic acids · 2025Review
- RasGRP4 aggravates ischemia-reperfusion injury in diabetic kidneys by mediating communication between macrophages and T cells.JCI insight · 2024Article
- Ras suppression potentiates rear actomyosin contractility-driven cell polarization and migration.Nature cell biology · 2024Article
- Article
- Nerve Growth Factor and Autoimmune Diseases.Current issues in molecular biology · 2023Review
- Actuation of single downstream nodes in growth factor network steers immune cell migration.Developmental cell · 2023Article
- Optogenetic modulation of guanine nucleotide exchange factors of Ras superfamily proteins directly controls cell shape and movement.Frontiers in cell and developmental biology · 2023Article
- Mutated RAS-associating proteins and ERK activation in relapse/refractory diffuse large B cell lymphoma.Scientific reports · 2022Article
- Ras inhibitors gate chemoattractant concentration range for chemotaxis through controlling GPCR-mediated adaptation and cell sensitivity.Frontiers in immunology · 2022Review
- Class I PI3K Biology.Current topics in microbiology and immunology · 2022Article
- Ras inhibitor CAPRI enables neutrophil-like cells to chemotax through a higher-concentration range of gradients.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Review
- Ras GEF Mouse Models for the Analysis of Ras Biology and Signaling.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Membrane Targeting of C2GAP1 EnablesFrontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
The molecular mechanisms by which receptors regulate the Ras Binding Domains of the PIP3-generating, class I PI3Ks remain poorly understood, despite their importance in a range of biological settings, including tumorigenesis, activation of neutrophils by pro-inflammatory mediators, chemotaxis of Dictyostelium and cell growth in Drosophila. We provide evidence that G protein-coupled receptors (GPCRs) can stimulate PLCb2/b3 and diacylglycerol- dependent activation of the RasGEF, RasGRP4 in neutrophils. The genetic loss of RasGRP4 phenocopies knock-in of a Ras-insensitive version of PI3Kc in its effects on PI3Kc-dependent PIP3 accumulation, PKB activation, chemokinesis and reactive oxygen species (ROS) formation. These results establish a new mechanism by which GPCRs can stimulate Ras, and the broadly important principle that PLCs can control activation of class I PI3Ks.
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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.