Evidence map›Paper›PMID 9763430›Full record

ArticleThe Journal of cell biology1998

Disruption of the NF-H gene increases axonal microtubule content and velocity of neurofilament transport: relief of axonopathy resulting from the toxin beta,beta'-iminodipropionitrile.

Q Zhu, M Lindenbaum, F Levavasseur, H Jacomy, J P Julien

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Neurofilaments and Neurofilament Proteins in Health and Disease.Cold Spring Harbor perspectives in biology · 2017
    Review
  10. MotomiRs: miRNAs in Motor Neuron Function and Disease.Frontiers in molecular neuroscience · 2017
    Review
  11. Article
  12. Article
  13. PGC-1α provides a transcriptional framework for synchronous neurotransmitter release from parvalbumin-positive interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  14. Article
  15. Neurofilamentopathy in neurodegenerative diseases.The open neurology journal · 2011
    Article
  16. Article
  17. Article
  18. Neurofilaments bind tubulin and modulate its polymerization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Q ZhuCentre for Research in Neuroscience, McGill University, The Montreal General Hospital Research Institute, Montréal, Qúebec, Canada H3G 1A4.
M Lindenbaum
F Levavasseur
H Jacomy
J P Julien
Montreal General Hospital · CAMcGill University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate the role of the neurofilament heavy (NF-H) subunit in neuronal function, we generated mice bearing a targeted disruption of the gene coding for the NF-H subunit. Surprisingly, the lack of NF-H subunits had little effect on axonal calibers and electron microscopy revealed no significant changes in the number and packing density of neurofilaments made up of only the neurofilament light (NF-L) and neurofilament medium (NF-M) subunits. However, our analysis of NF-H knockout mice revealed an approximately 2.4-fold increase of microtubule density in their large ventral root axons. This finding was further corroborated by a corresponding increase in the ratio of assembled tubulin to NF-L protein in insoluble cytoskeletal preparations from the sciatic nerve. Axonal transport studies carried out by the injection of [35S]methionine into spinal cord revealed an increased transport velocity of newly synthesized NF-L and NF-M proteins in motor axons of NF-H knockout mice. When treated with beta,beta'-iminodipropionitrile (IDPN), a neurotoxin that segregates microtubules and retards neurofilament transport, mice heterozygous or homozygous for the NF-H null mutation did not develop neurofilamentous swellings in motor neurons, unlike normal mouse littermates. These results indicate that the NF-H subunit is a key mediator of IDPN-induced axonopathy.

Indexed as

Actin CytoskeletonAnimalsAxonsExonsGanglia, SpinalMiceMice, KnockoutMicrotubulesNerve Fibers, MyelinatedNeurofilament ProteinsNeurotoxinsNitriles3,3'-iminodipropionitrileneurofilament protein Hneurofilament protein Lneurofilament protein MNeurofilament ProteinsNeurotoxinsNitriles

Identifiers

PMID9763430
PMCPMC2132812
OpenAlexW1987277509

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.