Evidence map›Paper›PMID 29974666›Full record

ArticleJournal of cellular and molecular medicine2018

Signalling through Src family kinase isoforms is not redundant in models of thrombo-inflammatory vascular disease.

Matthew J Harrison, Myriam Chimen, Mohammed Hussain, Asif J Iqbal, Yotis A Senis, Gerard B Nash, Steve P Watson, G Ed Rainger

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Matthew J HarrisonInstitute of Cardiovascular Sciences, College of Medical and Dental Science, The Medical School, University of Birmingham, Birmingham, UK.
Myriam ChimenInstitute of Cardiovascular Sciences, College of Medical and Dental Science, The Medical School, University of Birmingham, Birmingham, UK.ORCID 0000-0002-3567-1731
Mohammed HussainInstitute of Cardiovascular Sciences, College of Medical and Dental Science, The Medical School, University of Birmingham, Birmingham, UK.
Asif J IqbalInstitute of Cardiovascular Sciences, College of Medical and Dental Science, The Medical School, University of Birmingham, Birmingham, UK.
Yotis A SenisInstitute of Cardiovascular Sciences, College of Medical and Dental Science, The Medical School, University of Birmingham, Birmingham, UK.
Gerard B NashInstitute of Cardiovascular Sciences, College of Medical and Dental Science, The Medical School, University of Birmingham, Birmingham, UK.
Steve P WatsonInstitute of Cardiovascular Sciences, College of Medical and Dental Science, The Medical School, University of Birmingham, Birmingham, UK.
G Ed RaingerInstitute of Cardiovascular Sciences, College of Medical and Dental Science, The Medical School, University of Birmingham, Birmingham, UK.
University of Birmingham · GB

Funding

British Heart Foundation FS/14/42/30956British Heart Foundation PG/08/033/24856British Heart Foundation PG/11/49/28983British Heart Foundation RG/12/7/29693British Heart Foundation RG/15/13/31673
6 · The paper itself

Abstract

The Src family kinases (SFK) are a group of signalling molecules with important regulatory functions in inflammation and haemostasis. Leucocytes and platelets express multiple isoforms of the SFKs. Previous studies used broad-spectrum pharmacological inhibitors, or murine models deficient in multiple SFK isoforms, to demonstrate the functional consequences of deficiencies in SFK signalling. Here, we hypothesized that individual SFK operate in a non-redundant fashion in the thrombo-inflammatory recruitment of monocyte during atherosclerosis. Using in vitro adhesion assays and single SFK knockout mice crossed with the ApoE

Indexed as

AnimalsAortaApolipoproteins ECell AdhesionCoronary Artery DiseaseDiet, High-FatFemaleGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, Inbred C57BLMice, KnockoutMonocytesPrimary Cell CultureApolipoproteins Elyn protein-tyrosine kinaseProto-Oncogene Proteinsproto-oncogene proteins c-fgrsrc-Family KinasesatherosclerosisinflammationmonocytesplateletsSrc family kinases

Identifiers

PMID29974666
PMCPMC6111872
OpenAlexW2810200489

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.