Evidence map›Paper›PMID 9636192›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Resistance to endotoxic shock and reduced neutrophil migration in mice deficient for the Src-family kinases Hck and Fgr.

C A Lowell, G Berton

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

56 citing papers in PubMed, 179 citations in OpenAlex.

  1. Article
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  8. HCK maintains the self-renewal of leukaemia stem cells via CDK6 in AML.Journal of experimental & clinical cancer research : CR · 2021
    Article
  9. Article
  10. Article
  11. Expression of a Constitutively Active Form ofInternational journal of molecular sciences · 2020
    Article
  12. Neutrophils as emerging therapeutic targets.Nature reviews. Drug discovery · 2020
    Review
  13. Article
  14. International journal of medical sciences · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors at 2 institutions in 2 countries.

C A LowellDepartment of Laboratory Medicine, University of California, San Francisco, CA 94143-0100, USA. clowell@cgl.ucsf.edu
G Berton
University of California, San Francisco · USUniversity of Verona · IT

Funding

TYROSINE KINASES AND B LYMPHOCYTE TOLERANCEP50HL054476 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI BUSCH, MICHAEL PAUL · 1996 to 2005
$9.8M
THROMBIN RECEPTOR'S ROLE IN PLATELET AND MEGAKARYOCYTE BIOLOGYP01DK050267 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI LOWELL, CLIFFORD A · 1995 to 1999
–
NHLBI NIH HHS HL54476NHLBI NIH HHS P50 HL054476NIDDK NIH HHS DK50267
6 · The paper itself

Abstract

Signal transduction through the leukocyte integrins is required for the processes of firm adhesion, activation, and chemotaxis of neutrophils during inflammatory reactions. Neutrophils isolated from knockout mice that are deficient in the expression of p59/61(hck) (Hck) and p58(c-fgr) (Fgr), members of the Src-family of protein tyrosine kinases, have been shown to be defective in adhesion mediated activation. Cells from these animals have impaired induction of respiratory burst and granule secretion following plating on surfaces that crosslink beta2 and beta3 integrins. To determine if the defective function of hck-/-fgr-/- neutrophils observed in vitro also results in impaired inflammatory responses in vivo, we examined responses induced by lipopolysaccharide (LPS) injection in these animals. The hck-/-fgr-/- mice showed marked resistance to the lethal effects of high-dose LPS injection despite the fact that high levels of serum tumor necrosis factor alpha and interleukin 1alpha were detected. Serum chemistry analysis revealed a marked reduction in liver and renal damage in mutant mice treated with LPS, whereas blood counts showed a marked neutrophilia that was not seen in wild-type animals. Direct examination of liver sections from mutant mice revealed reduced neutrophil migration into the tissue. These data demonstrate that defective integrin signaling in neutrophils, caused by loss of Hck and Fgr tyrosine kinase activity, results in impaired inflammation-dependent tissue injury in vivo.

Indexed as

AnimalsCell AdhesionChemotaxis, LeukocyteImmunity, InnateLipopolysaccharidesLiverMiceMice, Inbred C57BLNeutrophilsProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-hckShock, SepticSignal Transductionsrc-Family KinasesHck protein, mouseLipopolysaccharidesProtein-Tyrosine KinasesProto-Oncogene Proteinsproto-oncogene proteins c-fgrProto-Oncogene Proteins c-hcksrc-Family Kinases

Identifiers

PMID9636192
PMCPMC22689
OpenAlexW2047517330

What OpenQuestion holds

Textmetadata
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.