Evidence map›Paper›PMID 30720883›Full record

ArticleJournal of leukocyte biology2019

Frontline Science: TNF-α and GM-CSF1 priming augments the role of SOS1/2 in driving activation of Ras, PI3K-γ, and neutrophil proinflammatory responses.

Sabine Suire, Fernando C Baltanas, Anne Segonds-Pichon, Keith Davidson, Eugenio Santos, Phillip T Hawkins, Len R Stephens

Open access · hybridAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. 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 · 2025
    Article
  3. SOS1 inhibitor BI-3406 shows in vivo antitumor activity akin to genetic ablation and synergizes with a KRASProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  14. Review
  15. Article
  16. Ras GEF Mouse Models for the Analysis of Ras Biology and Signaling.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Sabine SuireInositide Laboratory, The Babraham Institute, Cambridge, UK.
Fernando C BaltanasCentro de Investigación del Cáncer-Instituto de Biología Molecular y Celular del Cáncer, (CSIC- Universitad de Salamanca) and CiberONC, Salamanca, Spain.
Anne Segonds-PichonBioinformatics Group, The Babraham Institute, Cambridge, UK.
Keith DavidsonInositide Laboratory, The Babraham Institute, Cambridge, UK.
Eugenio SantosCentro de Investigación del Cáncer-Instituto de Biología Molecular y Celular del Cáncer, (CSIC- Universitad de Salamanca) and CiberONC, Salamanca, Spain.
Phillip T HawkinsInositide Laboratory, The Babraham Institute, Cambridge, UK.
Len R StephensInositide Laboratory, The Babraham Institute, Cambridge, UK.
Babraham Institute · GBCentro de Investigación del Cáncer · ES

Funding

Biotechnology and Biological Sciences Research Council BB/J004456/1Biotechnology and Biological Sciences Research Council BB/P013384/1Biotechnology and Biological Sciences Research Council BBS/E/B/000C0411Medical Research Council MR/K018167/1
6 · The paper itself

Abstract

Circulating neutrophils are, by necessity, quiescent and relatively unresponsive to acute stimuli. In regions of inflammation, mediators can prime neutrophils to react to acute stimuli with stronger proinflammatory, pathogen-killing responses. In neutrophils G protein-coupled receptor (GPCR)-driven proinflammatory responses, such as reactive oxygen species (ROS) formation and accumulation of the key intracellular messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP

Indexed as

AnimalsEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGranulocyte-Macrophage Colony-Stimulating FactorInflammationMiceNeutrophilsN-Formylmethionine Leucyl-PhenylalaninePhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhospholipase C betaras Guanine Nucleotide Exchange Factorsras ProteinsReactive Oxygen SpeciesSignal TransductionSon of Sevenless ProteinsExtracellular Signal-Regulated MAP KinasesGranulocyte-Macrophage Colony-Stimulating FactorN-Formylmethionine Leucyl-PhenylalaninePhosphatidylinositol 3-Kinasesphosphatidylinositol 3-phosphatePhosphatidylinositol PhosphatesPhospholipase C betaRasgrp4 protein, mouseras Guanine Nucleotide Exchange Factorsras ProteinsReactive Oxygen SpeciesSon of Sevenless ProteinsSOS1 ProteinSos2 protein, mouseTumor Necrosis Factor-alphaPI3KRasGEFSOS

Identifiers

PMID30720883
PMCPMC6977543
OpenAlexW2913587782

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.