Evidence map›Paper›PMID 22291096›Full record

ArticleThe Journal of experimental medicine2012

Crucial role of SLP-76 and ADAP for neutrophil recruitment in mouse kidney ischemia-reperfusion injury.

Helena Block, Jan M Herter, Jan Rossaint, Anika Stadtmann, Stefanie Kliche, Clifford A Lowell, Alexander Zarbock

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

64 citing papers in PubMed, 98 citations in OpenAlex.

  1. Trial
  2. Review
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  7. Article
  8. Review
  9. Neutrophils-biology and diversity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  10. Article
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  12. Article
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  18. Article
  19. Article
  20. Mired in the glomeruli: witnessing live neutrophil recruitment in the kidney.American journal of physiology. Cell physiology · 2021
    Review

4 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

7 authors at 4 institutions in 2 countries.

Helena BlockDepartment of Anesthesiology and Critical Care Medicine, University of Münster, 48149 Münster, Germany.
Jan M Herter
Jan Rossaint
Anika Stadtmann
Stefanie Kliche
Clifford A Lowell
Alexander Zarbock
University of Münster · DEMax Planck Institute for Molecular Biomedicine · DEOtto-von-Guericke University Magdeburg · DEUniversity of California, San Francisco · US

Funding

Signaling by Cytoplasmic Tyrosine Kinases in LeukocytesR01AI068150 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2006 to 2016
$3.4M
NIAID NIH HHS R01 AI068150
6 · The paper itself

Abstract

Neutrophils trigger inflammation-induced acute kidney injury (AKI), a frequent and potentially lethal occurrence in humans. Molecular mechanisms underlying neutrophil recruitment to sites of inflammation have proved elusive. In this study, we demonstrate that SLP-76 (SH2 domain-containing leukocyte phosphoprotein of 76 kD) and ADAP (adhesion and degranulation promoting adaptor protein) are involved in E-selectin-mediated integrin activation and slow leukocyte rolling, which promotes ischemia-reperfusion-induced AKI in mice. By using genetically engineered mice and transduced Slp76(-/-) primary leukocytes, we demonstrate that ADAP as well as two N-terminal-located tyrosines and the SH2 domain of SLP-76 are required for downstream signaling and slow leukocyte rolling. The Tec family kinase Bruton tyrosine kinase is downstream of SLP-76 and, together with ADAP, regulates PI3Kγ (phosphoinositide 3-kinase-γ)- and PLCγ2 (phospholipase Cγ2)-dependent pathways. Blocking both pathways completely abolishes integrin affinity and avidity regulation. Thus, SLP-76 and ADAP are involved in E-selectin-mediated integrin activation and neutrophil recruitment to inflamed kidneys, which may underlie the development of life-threatening ischemia-reperfusion-induced AKI in humans.

Indexed as

Adaptor Proteins, Signal TransducingAgammaglobulinaemia Tyrosine KinaseAnimalsCell Line, TumorClass Ib Phosphatidylinositol 3-KinaseE-SelectinGenetic VectorsHumansIntegrinsKidneyLeukocyte RollingMiceMice, Inbred C57BLMice, TransgenicNeutrophilsPeritonitisAdaptor Proteins, Signal TransducingAgammaglobulinaemia Tyrosine KinaseBtk protein, mouseClass Ib Phosphatidylinositol 3-KinaseE-SelectinFyb protein, mouseIntegrinsPhospholipase C gammaPhosphoproteinsPik3cg protein, mouseProtein-Tyrosine KinasesSLP-76 signal Transducing adaptor proteinsThioglycolates

Identifiers

PMID22291096
PMCPMC3280874
OpenAlexW2007980002

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.