Evidence map›Paper›PMID 9832557›Full record

ArticleThe Journal of cell biology1998

AnkyrinG is required for clustering of voltage-gated Na channels at axon initial segments and for normal action potential firing.

D Zhou, S Lambert, P L Malen, S Carpenter, L M Boland, V Bennett

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 311 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
311citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

311 citing papers in PubMed, 1 synthesis or guideline pooled it, 568 citations in OpenAlex.

  1. Pooled it
  2. Article
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  7. Review
  8. Article
  9. Reframing the axon initial segment: Giant ankyrin-G as a modulator of excitability and plasticity in neurodevelopment.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Review
  11. Hippocampal Chandelier Cells Modulate Seizure Susceptibility and Severity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  12. A neuron type-specific microexon inbioRxiv : the preprint server for biology · 2025
    Article
  13. Impaired AIS plasticity in ankyrin-G mutant mice alters cortical excitability and behavior.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Loss of ANK3 Function Causes a Recessive Neurodevelopmental Disorder with Cerebellar Ataxia.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
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  20. Review

251 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

D ZhouHoward Hughes Medical Institute and Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
S Lambert
P L Malen
S Carpenter
L M Boland
V Bennett
University of Massachusetts Chan Medical School · USUniversity of Minnesota Medical Center · USDuke Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Voltage-gated sodium channels (NaCh) are colocalized with isoforms of the membrane-skeletal protein ankyrinG at axon initial segments, nodes of Ranvier, and postsynaptic folds of the mammalian neuromuscular junction. The role of ankyrinG in directing NaCh localization to axon initial segments was evaluated by region-specific knockout of ankyrinG in the mouse cerebellum. Mutant mice exhibited a progressive ataxia beginning around postnatal day P16 and subsequent loss of Purkinje neurons. In mutant mouse cerebella, NaCh were absent from axon initial segments of granule cell neurons, and Purkinje cells showed deficiencies in their ability to initiate action potentials and support rapid, repetitive firing. Neurofascin, a member of the L1CAM family of ankyrin-binding cell adhesion molecules, also exhibited impaired localization to initial segments of Purkinje cell neurons. These results demonstrate that ankyrinG is essential for clustering NaCh and neurofascin at axon initial segments and is required for physiological levels of sodium channel activity.

Indexed as

Action PotentialsAmino Acid SequenceAnimalsAnkyrinsAtaxiaAxonsBase SequenceCell Adhesion MoleculesCerebellumMiceMice, Inbred C57BLMice, KnockoutMolecular Sequence DataNerve DegenerationNerve Growth FactorsOligonucleotide ProbesAnkyrinsCell Adhesion MoleculesNerve Growth FactorsNfasc protein, mouseOligonucleotide ProbesSodium Channels

Identifiers

PMID9832557
PMCPMC2133082
OpenAlexW2164425582

What OpenQuestion holds

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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.