Evidence map›Paper›PMID 15249579›Full record

ArticleThe Journal of cell biology2004

Vav GEFs are required for beta2 integrin-dependent functions of neutrophils.

M Angelica Martinez Gakidis, Xavier Cullere, Timothy Olson, Julie L Wilsbacher, Bin Zhang, Sheri L Moores, Klaus Ley, Wojciech Swat, Tanya Mayadas, Joan S Brugge

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
7.9field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 221 citations in OpenAlex.

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  15. Review
  16. Rac-GTPases and Rac-GEFs in neutrophil adhesion, migration and recruitment.European journal of clinical investigation · 2018
    Review
  17. Article
  18. Review
  19. Review
  20. Article

31 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 1 country.

M Angelica Martinez GakidisDepartment of Cell Biology, Harvard Medical School, 240 Longwood Ave., Boston, MA 02115, USA.
Xavier Cullere
Timothy Olson
Julie L Wilsbacher
Bin Zhang
Sheri L Moores
Klaus Ley
Wojciech Swat
Tanya Mayadas
Joan S Brugge
Harvard University · USBrigham and Women's Hospital · USUniversity of Virginia · USWashington University in St. Louis · US

Funding

VCAM-1 IN CHRONIC INFLAMMATORY AND IMMUNE PROCESSESP01HL036028 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LUSCINSKAS, FRANCIS W. · 1985 to 2013
$32.1M
WIP in TCR signaling and actin reorganizationP01HL059561 · NHLBI · IMMUNE DISEASE INSTITUTE, INC. · PI GEHA, RAIF SALIM · 1997 to 2012
$21.8M
Regulators of Immune Complex Mediated Neutrophil Recruitment and Tissue InjuryR01HL065095 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI MAYADAS, TANYA N · 1999 to 2025
$11.9M
SIGNAL TRANSDUCTION EVENTS REGULATED BY INTEGRINSR01CA078773 · NCI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BRUGGE, JOAN SIEFERT · 1998 to 2003
$1.7M
NCI NIH HHS CA78773NCI NIH HHS R01 CA078773NHLBI NIH HHS HL059561NHLBI NIH HHS HL36028NHLBI NIH HHS HL65095NHLBI NIH HHS P01 HL036028NHLBI NIH HHS P01 HL059561NHLBI NIH HHS R01 HL065095
6 · The paper itself

Abstract

Integrin regulation of neutrophils is essential for appropriate adhesion and transmigration into tissues. Vav proteins are Rho family guanine nucleotide exchange factors that become tyrosine phosphorylated in response to adhesion. Using Vav1/Vav3-deficient neutrophils (Vav1/3ko), we show that Vav proteins are required for multiple beta2 integrin-dependent functions, including sustained adhesion, spreading, and complement-mediated phagocytosis. These defects are not attributable to a lack of initial beta2 activation as Vav1/3ko neutrophils undergo chemoattractant-induced arrest on intercellular adhesion molecule-1 under flow. Accordingly, in vivo, Vav1/3ko leukocytes arrest on venular endothelium yet are unable to sustain adherence. Thus, Vav proteins are specifically required for stable adhesion. beta2-induced activation of Cdc42, Rac1, and RhoA is defective in Vav1/3ko neutrophils, and phosphorylation of Pyk2, paxillin, and Akt is also significantly reduced. In contrast, Vav proteins are largely dispensable for G protein-coupled receptor-induced signaling events and chemotaxis. Thus, Vav proteins play an essential role coupling beta2 to Rho GTPases and regulating multiple integrin-induced events important in leukocyte adhesion and phagocytosis.

Indexed as

Cell Cycle ProteinsAnimalsCD18 AntigensCell AdhesionChemotaxis, LeukocyteEndothelium, VascularGuanine Nucleotide Exchange FactorsMiceMice, KnockoutNeutrophilsOncogene ProteinsPhagocytosisProto-Oncogene ProteinsProto-Oncogene Proteins c-vavrho GTP-Binding ProteinsSignal TransductionCD18 AntigensCell Cycle ProteinsGuanine Nucleotide Exchange FactorsOncogene ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-vavrho GTP-Binding ProteinsVav1 protein, mouseVav2 protein, mouseVav3 protein, mouse

Identifiers

PMID15249579
PMCPMC2172310
OpenAlexW2137850515

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.