Evidence map›Paper›PMID 24563812›Full record

ArticleJournal of genetic syndromes & gene therapy2013

Microtubule defects & Neurodegeneration.

Fiona J Baird, Craig L Bennett

Open access · greenAbstract read
In one paragraph

Article in Journal of genetic syndromes & gene therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

33 citing papers in PubMed, 48 citations in OpenAlex.

  1. Neuronal Calcium Signaling and Cytoskeletal Dynamics in Neurodegeneration.International journal of molecular sciences · 2026
    Review
  2. PolyQ-Expansion of Ataxin-2 Disrupts Microtubule Stability and Impairs Axon Outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Binding Parameters of [Pharmaceuticals (Basel, Switzerland) · 2023
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. NovelNeurology. Genetics · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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 1 institution in 1 country.

Fiona J BairdSchool of Pharmacy and Molecular Sciences, James Cook University, DB 21, James Cook Drive, Townsville, QLD 4811, Australia ; Centre of Biodiscovery and Molecular Therapeutics, James Cook University, DB 21, James Cook Drive, Townsville, QLD 4811, Australia.
Craig L BennettSchool of Pharmacy and Molecular Sciences, James Cook University, DB 21, James Cook Drive, Townsville, QLD 4811, Australia ; Department of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA.
James Cook University · AU

Funding

Neuronal RNA processing defects in ALS4 caused by SETX mutationsR01GM094384 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BENNETT, CRAIG L · 2010 to 2014
$1.5M
NIGMS NIH HHS R01 GM094384
6 · The paper itself

Abstract

One of the major challenges facing the long term survival of neurons is their requirement to maintain efficient axonal transport over long distances. In humans as large, long-lived vertebrates, the machinery maintaining neuronal transport must remain efficient despite the slow accumulation of cell damage during aging. Mutations in genes encoding proteins which function in the transport system feature prominently in neurologic disorders. Genes known to cause such disorders and showing traditional Mendelian inheritance have been more readily identified. It has been more difficult, however, to isolate factors underlying the complex genetics contributing to the more common idiopathic forms of neurodegenerative disease. At the heart of neuronal transport is the rail network or scaffolding provided by neuron specific microtubules (MTs). The importance of MT dynamics and stability is underscored by the critical role tau protein plays in MT-associated stabilization versus the dysfunction seen in Alzheimer's disease, frontotemporal dementia and other tauopathies. Another example of the requirement for tight regulation of MT dynamics is the need to maintain balanced levels of post-translational modification of key MT building-blocks such as α-tubulin. Tubulins require extensive polyglutamylation at their carboxyl-terminus as part of a novel post-translational modification mechanism to signal MT growth versus destabilization. Dramatically, knock-out of a gene encoding a deglutamylation family member causes an extremely rapid cell death of Purkinje cells in the ataxic mouse model,

Identifiers

PMID24563812
PMCPMC3930179
OpenAlexW2033815272

What OpenQuestion holds

Textmetadata
LicenceTDM
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.