Evidence map›Paper›PMID 17614878›Full record

ReviewImmunology2007

Phosphoinositide 3-kinase signalling in lung disease: leucocytes and beyond.

David A Medina-Tato, Stephen G Ward, Malcolm L Watson

Open access · greenAbstract readReview
In one paragraph

Review in Immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
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  10. TGFβ as a therapeutic target in cystic fibrosis.Expert opinion on therapeutic targets · 2018
    Review
  11. Lignans Isolated From Flower Buds ofFrontiers in pharmacology · 2018
    Article
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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

3 authors at 1 institution in 1 country.

David A Medina-TatoDepartment of Pharmacy & Pharmacology, University of Bath, Bath, UK.
Stephen G Ward
Malcolm L Watson
University of Bath · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The family of lipid kinases termed phosphoinositide-3-kinase (PI3K) is known to contribute at multiple levels to innate and adaptive immune responses, and is hence an attractive target for drug discovery in inflammatory and autoimmune disease, including respiratory diseases. The development of isoform-selective pharmacological inhibitors, targeted gene manipulation and short interfering RNA (siRNA) target validation have facilitated a better understanding of the role that each member of this family of kinases plays in the physiology and pathology of the respiratory system. In this review, we will evaluate the evidence for the roles of specific PI3K isoforms in the lung and airways, and discuss their potential as targets for novel drug therapies.

Indexed as

AsthmaHumansLeukocytesLung DiseasesPhosphatidylinositol 3-KinasesProtein IsoformsPulmonary Disease, Chronic ObstructiveRespiratory Distress SyndromeSignal TransductionPhosphatidylinositol 3-KinasesProtein Isoforms

Identifiers

PMID17614878
PMCPMC2265972
OpenAlexW2059870548

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.