Evidence map›Paper›PMID 28034912›Full record

ReviewPharmacological reviews2017

Pharmacology of Modulators of Alternative Splicing.

David O Bates, Jonathan C Morris, Sebastian Oltean, Lucy F Donaldson

Open access · bronzeAbstract readReview
In one paragraph

Review in Pharmacological reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 84 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

4 authors at 3 institutions in 2 countries.

David O BatesCancer Biology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom (D.O.B.); School of Chemistry, UNSW Australia, Sydney, Australia (J.C.M.); School of Physiology, Pharmacology and Neurosciences, School of Clinical Sciences/Bristol Renal, University of Bristol, Bristol, United Kingdom (S.O.); and School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom (L.F.D.) David.Bates@nottingham.ac.uk.
Jonathan C MorrisCancer Biology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom (D.O.B.); School of Chemistry, UNSW Australia, Sydney, Australia (J.C.M.); School of Physiology, Pharmacology and Neurosciences, School of Clinical Sciences/Bristol Renal, University of Bristol, Bristol, United Kingdom (S.O.); and School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom (L.F.D.).
Sebastian OlteanCancer Biology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom (D.O.B.); School of Chemistry, UNSW Australia, Sydney, Australia (J.C.M.); School of Physiology, Pharmacology and Neurosciences, School of Clinical Sciences/Bristol Renal, University of Bristol, Bristol, United Kingdom (S.O.); and School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom (L.F.D.).
Lucy F DonaldsonCancer Biology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom (D.O.B.); School of Chemistry, UNSW Australia, Sydney, Australia (J.C.M.); School of Physiology, Pharmacology and Neurosciences, School of Clinical Sciences/Bristol Renal, University of Bristol, Bristol, United Kingdom (S.O.); and School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom (L.F.D.).
University of Nottingham · GBUniversity of Bristol · GBUNSW Sydney · AU

Funding

British Heart Foundation PG/15/53/31371Medical Research Council MR/K013157/1Medical Research Council MR/K020366/1Medical Research Council MR/N01247X/1
6 · The paper itself

Abstract

More than 95% of genes in the human genome are alternatively spliced to form multiple transcripts, often encoding proteins with differing or opposing function. The control of alternative splicing is now being elucidated, and with this comes the opportunity to develop modulators of alternative splicing that can control cellular function. A number of approaches have been taken to develop compounds that can experimentally, and sometimes clinically, affect splicing control, resulting in potential novel therapeutics. Here we develop the concepts that targeting alternative splicing can result in relatively specific pathway inhibitors/activators that result in dampening down of physiologic or pathologic processes, from changes in muscle physiology to altering angiogenesis or pain. The targets and pharmacology of some of the current inhibitors/activators of alternative splicing are demonstrated and future directions discussed.

Indexed as

Molecular Targeted TherapyAlternative SplicingAnimalsDrug DiscoveryGene Expression RegulationHumansRNASignal TransductionTranscription, GeneticRNA

Identifiers

PMID28034912
PMCPMC5226212
OpenAlexW2562883249

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.