Evidence map›Paper›PMID 9294149›Full record

ArticleThe Journal of experimental medicine1997

Rho is required for the initiation of calcium signaling and phagocytosis by Fcgamma receptors in macrophages.

D J Hackam, O D Rotstein, A Schreiber, W j Zhang, S Grinstein

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

53 citing papers in PubMed, 165 citations in OpenAlex.

  1. Article
  2. Convergence of Ras- and Rac-regulated formin pathways is pivotal for phagosome formation and particle uptake inProceedings of the National Academy of Sciences of the United States of America · 2023
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  11. Endothelium-neutrophil interactions in ANCA-associated diseases.Journal of the American Society of Nephrology : JASN · 2012
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  14. DNA attenuates enterocyte Toll-like receptor 4-mediated intestinal mucosal injury after remote trauma.American journal of physiology. Gastrointestinal and liver physiology · 2011
    Article
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  17. Mechanisms of failed apoptotic cell clearance by phagocyte subsets in cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2010
    Review
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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

5 authors at 2 institutions in 2 countries.

D J HackamDivision of Cell Biology, Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada.
O D Rotstein
A Schreiber
W j Zhang
S Grinstein
University of Pennsylvania · USHospital for Sick Children · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phagocytosis of bacteria by macrophages and neutrophils is an essential component of host defense against infection. The mechanism whereby the interaction of opsonized particles with Fcgamma receptors triggers the engulfment of opsonized particles remains incompletely understood, although activation of tyrosine kinases has been recognized as an early step. Recent studies in other systems have demonstrated that tyrosine kinases can in turn signal the activation of small GTPases of the ras superfamily. We therefore investigated the possible role of Rho in Fc receptor-mediated phagocytosis. To this end we microinjected J774 macrophages with C3 exotoxin from Clostridium botulinum, which ADP-ribosylates and inactivates Rho. C3 exotoxin induced the retraction of filopodia, the disappearance of focal complexes, and a global decrease in the F-actin content of J774 cells. In addition, these cells exhibited increased spreading and the formation of vacuolar structures. Importantly, inactivation of Rho resulted in the complete abrogation of phagocytosis. Inhibition of Fcgamma receptor-mediated phagocytosis by C3 exotoxin was confirmed in COS cells, which become phagocytic upon transfection of the FcgammaRIIA receptor. Rho was found to be essential for the accumulation of phosphotyrosine and of F-actin around phagocytic cups and for Fcgamma receptor-mediated Ca2+ signaling. The clustering of receptors in response to opsonin, an essential step in Fcgamma-induced signaling, was the earliest event shown to be inhibited by C3 exotoxin. The effect of the toxin was specific, since clustering and internalization of transferrin receptors were unaffected by microinjection of C3. These data identify a role for small GTPases in Fcgamma receptor-mediated phagocytosis by leukocytes.

Indexed as

ActinsAnimalsBotulinum ToxinsCalciumCell LineCOS CellsExotoxinsGTP-Binding ProteinsHydrogen-Ion ConcentrationMacrophagesMembrane ProteinsMicePhagocytosisPhosphotyrosineReceptors, IgGrhoB GTP-Binding ProteinActinsBotulinum Toxinsbotulinum toxin type CCalciumExotoxinsGTP-Binding ProteinsMembrane ProteinsPhosphotyrosineReceptors, IgGrhoB GTP-Binding Protein

Identifiers

PMID9294149
PMCPMC2199044
OpenAlexW2023497277

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.