Evidence map›Paper›PMID 14662746›Full record

ArticleThe Journal of cell biology2003

The neurofilament middle molecular mass subunit carboxyl-terminal tail domains is essential for the radial growth and cytoskeletal architecture of axons but not for regulating neurofilament transport rate.

Mala V Rao, Jabbar Campbell, Aidong Yuan, Asok Kumar, Takahiro Gotow, Yasuo Uchiyama, Ralph A Nixon

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2003. 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
2.5field-weighted citation impact, top 12% 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, 125 citations in OpenAlex.

  1. Increase of Plasma Biomarkers in Friedreich's Ataxia: Potential Insights into Disease Pathology.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  2. Review
  3. Article
  4. Dissecting neurofilament tail sequence-phosphorylation-structure relationships with multicomponent reconstituted protein brushes.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Neurofilaments in health and Charcot-Marie-Tooth disease.Frontiers in cell and developmental biology · 2023
    Review
  10. Review
  11. Article
  12. Studying Neuronal Biology Using Spinning Disc Confocal Microscopy.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
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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

7 authors at 4 institutions in 2 countries.

Mala V RaoNathan Kline Institute, NYU School of Medicine, 140 Old Orangeburg Rd., Orangeburg, NY 10962, USA. rao@nki.rfmh.org
Jabbar Campbell
Aidong Yuan
Asok Kumar
Takahiro Gotow
Yasuo Uchiyama
Ralph A Nixon
New York University · USKoshien University · JPNathan Kline Institute for Psychiatric Research · USOsaka University · JP

Funding

NEURONAL FILAMENT SYNTHESIS, ASSEMBLY, AND FUNCTIONR01NS027036 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bogdan Bintu, Don W Cleveland · 1989 to 2026
$11.8M
PHYSICAL ACTIVITY-EFFECTS ON ENERGY METABOLISMK04AG000564 · NIA · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI POEHLMAN, ERIC T. · 1992 to 1996
–
NIA NIH HHS AG0564NINDS NIH HHS R01 NS027036NINDS NIH HHS R01 NS 27036
6 · The paper itself

Abstract

The phosphorylated carboxyl-terminal "tail" domains of the neurofilament (NF) subunits, NF heavy (NF-H) and NF medium (NF-M) subunits, have been proposed to regulate axon radial growth, neurofilament spacing, and neurofilament transport rate, but direct in vivo evidence is lacking. Because deletion of the tail domain of NF-H did not alter these axonal properties (Rao, M.V., M.L. Garcia, Y. Miyazaki, T. Gotow, A. Yuan, S. Mattina, C.M. Ward, N.S. Calcutt, Y. Uchiyama, R.A. Nixon, and D.W. Cleveland. 2002. J. Cell Biol. 158:681-693), we investigated possible functions of the NF-M tail domain by constructing NF-M tail-deleted (NF-MtailDelta) mutant mice using an embryonic stem cell-mediated "gene knockin" approach that preserves normal ratios of the three neurofilament subunits. Mutant NF-MtailDelta mice exhibited severely inhibited radial growth of both motor and sensory axons. Caliber reduction was accompanied by reduced spacing between neurofilaments and loss of long cross-bridges with no change in neurofilament protein content. These observations define distinctive functions of the NF-M tail in regulating axon caliber by modulating the organization of the neurofilament network within axons. Surprisingly, the average rate of axonal transport of neurofilaments was unaltered despite these substantial effects on axon morphology. These results demonstrate that NF-M tail-mediated interactions of neurofilaments, independent of NF transport rate, are critical determinants of the size and cytoskeletal architecture of axons, and are mediated, in part, by the highly phosphorylated tail domain of NF-M.

Indexed as

AnimalsAxonal TransportAxonsCell DivisionCell SurvivalCytoskeletonGene TargetingMiceMice, TransgenicMicrotubulesMolecular WeightNeurofilament ProteinsProtein Structure, TertiaryProtein Subunitsneurofilament protein MNeurofilament ProteinsProtein Subunits

Identifiers

PMID14662746
PMCPMC2173612
OpenAlexW2109097355

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.