Evidence map›Paper›PMID 2121744›Full record

ArticleThe Journal of cell biology1990

Assembly properties of dominant and recessive mutations in the small mouse neurofilament (NF-L) subunit.

S R Gill, P C Wong, M J Monteiro, D W Cleveland

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 174 citations in OpenAlex.

  1. Chiral inversion mutagenesis identifies geometrically constrained residues within self-associating low-complexity domains.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Transiently structured head domains control intermediate filament assembly.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Review
  8. Vitamin DNeuromolecular medicine · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Neurofilaments form a highly stable stationary cytoskeleton after reaching a critical level in axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. An intact intermediate filament network is required for collateral sprouting of small diameter nerve fibers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  18. Untranslated element in neurofilament mRNA has neuropathic effect on motor neurons of transgenic mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  19. Article
  20. Bcl-2 overexpression does not protect neurons from mutant neurofilament-mediated motor neuron degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999
    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

4 authors at 1 institution in 1 country.

S R GillDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
P C Wong
M J Monteiro
D W Cleveland
Johns Hopkins Medicine · US

Funding

NEURONAL FILAMENT SYNTHESIS, ASSEMBLY, AND FUNCTIONR01NS027036 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bogdan Bintu, Don W Cleveland · 1989 to 2026
$11.8M
Neurofilaments, SOD1 and Motor Neuron DiseasesR37NS027036 · NINDS · LUDWIG INSTITUTE FOR CANCER RES LTD · PI CLEVELAND, DON W · 2005 to 2011
$4.1M
NINDS NIH HHS NS 27036
6 · The paper itself

Abstract

We have generated a set of amino- and carboxy-terminal deletions of the NF-L neurofilament gene and determined the assembly properties of the encoded subunits after coexpression with vimentin or wild-type NF-L. NF-L molecules missing greater than 30% (31 amino acids of the head) or 90% (128 amino acids of the tail) failed to incorporate into intermediate filament networks. Carboxy-terminal deletions into the rod domain yield dominant mutants that disrupt arrays assembled from wild-type subunits, even when present at levels of approximately 2% of the wild-type subunits. Even mutants retaining 55% of the tail (61 amino acids) disrupt normal arrays when accumulated above approximately 10% of wild-type subunits. Since deletion of greater than 90% of the head domain produces "recessive" assembly incompetent subunits that do not affect wild-type filament arrays, whereas smaller deletions yield efficient network disruption, we conclude that some sequence(s) in the head domain (within residues 31-87) are required for the earliest steps in filament assembly. Insertional mutagenesis in the nonhelical spacer region within the rod domain reveals that as many as eight additional amino acids can be tolerated without disrupting assembly competence.

Indexed as

Amino Acid SequenceAnimalsBase SequenceChromosome DeletionFluorescent Antibody TechniqueGenes, DominantGenes, RecessiveIntermediate Filament ProteinsIntermediate FilamentsL CellsMiceMolecular Sequence DataNeurofilament ProteinsStructure-Activity RelationshipTransfectionIntermediate Filament ProteinsNeurofilament Proteins

Identifiers

PMID2121744
PMCPMC2116331
OpenAlexW2052484237

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.