Evidence map›Paper›PMID 26972010›Full record

ArticleCell reports2016

Pharmacological Bypass of Cockayne Syndrome B Function in Neuronal Differentiation.

Yuming Wang, Jace Jones-Tabah, Probir Chakravarty, Aengus Stewart, Alysson Muotri, Rebecca R Laposa, Jesper Q Svejstrup

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Temporal Bone Histopathology in Cockayne Syndrome.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2018
    Article
  14. Review
  15. 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

7 authors at 5 institutions in 3 countries.

Yuming WangMechanisms of Transcription Laboratory, Clare Hall Laboratories, The Francis Crick Institute, South Mimms, Hertfordshire EN6 3LD, UK.
Jace Jones-TabahDepartment of Pharmacology and Toxicology, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.
Probir ChakravartyBioinformatics & Biostatistics Group, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Aengus StewartBioinformatics & Biostatistics Group, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Alysson MuotriDepartment of Pediatrics, University of California, San Diego, 2800 Torrey Pines Scenic Drive, La Jolla, CA 92037, USA; Department of Cellular and Molecular Medicine, University of California, San Diego, 2800 Torrey Pines Scenic Drive, La Jolla, CA 92037, USA.
Rebecca R LaposaDepartment of Pharmacology and Toxicology, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.
Jesper Q SvejstrupMechanisms of Transcription Laboratory, Clare Hall Laboratories, The Francis Crick Institute, South Mimms, Hertfordshire EN6 3LD, UK. Electronic address: jesper.svejstrup@crick.ac.uk.
The Francis Crick Institute · GBCanada Research Chairs · CAThe Honourable Society of Lincoln's Inn · GBTorrey Pines Institute For Molecular Studies · USUniversity of Toronto · CA

Funding

Cancer Research UK 11567Medical Research CouncilWellcome Trust
6 · The paper itself

Abstract

Cockayne syndrome (CS) is a severe neurodevelopmental disorder characterized by growth abnormalities, premature aging, and photosensitivity. Mutation of Cockayne syndrome B (CSB) affects neuronal gene expression and differentiation, so we attempted to bypass its function by expressing downstream target genes. Intriguingly, ectopic expression of Synaptotagmin 9 (SYT9), a key component of the machinery controlling neurotrophin release, bypasses the need for CSB in neuritogenesis. Importantly, brain-derived neurotrophic factor (BDNF), a neurotrophin implicated in neuronal differentiation and synaptic modulation, and pharmacological mimics such as 7,8-dihydroxyflavone and amitriptyline can compensate for CSB deficiency in cell models of neuronal differentiation as well. SYT9 and BDNF are downregulated in CS patient brain tissue, further indicating that sub-optimal neurotrophin signaling underlies neurological defects in CS. In addition to shedding light on cellular mechanisms underlying CS and pointing to future avenues for pharmacological intervention, these data suggest an important role for SYT9 in neuronal differentiation.

Indexed as

AmitriptylineBrain-Derived Neurotrophic FactorCell DifferentiationCell Line, TumorChromatin ImmunoprecipitationCockayne SyndromeDNA HelicasesDNA Repair EnzymesDown-RegulationFlavonesHumansMembrane GlycoproteinsMicroscopy, FluorescencePoly-ADP-Ribose Binding ProteinsProtein-Tyrosine KinasesReal-Time Polymerase Chain Reaction6,7-dihydroxyflavoneAmitriptylineBDNF protein, humanBrain-Derived Neurotrophic FactorDNA HelicasesDNA Repair EnzymesERCC6 protein, humanFlavonesMembrane GlycoproteinsPoly-ADP-Ribose Binding ProteinsProtein-Tyrosine KinasesReceptor, trkBRNA, Small InterferingSynaptotagminsSYT9 protein, humantropomyosin-related kinase-B, human

Identifiers

PMID26972010
PMCPMC4806223
OpenAlexW2293936410

What OpenQuestion holds

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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.