Evidence map›Paper›PMID 30723396›Full record

ArticleFrontiers in cellular neuroscience2019

Loss of Neurofascin-186 Disrupts Alignment of AnkyrinG Relative to Its Binding Partners in the Axon Initial Segment.

Scott A Alpizar, Arielle L Baker, Allan T Gulledge, Michael B Hoppa

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
7.0field-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

17 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Live imaging of excitable axonal microdomains in ankyrin-G-GFP mice.bioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Extracellular Tau Oligomers Damage the Axon Initial Segment.Journal of Alzheimer's disease : JAD · 2023
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. The potassium channel subunit KProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Article
  15. Article
  16. Ataxia in Patients With Bi-AllelicFrontiers in genetics · 2019
    Article
  17. 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.

Scott A AlpizarDepartment of Biological Sciences, Dartmouth College, Hanover, NH, United States.
Arielle L BakerDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth College, Hanover, NH, United States.
Allan T GulledgeDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth College, Hanover, NH, United States.
Michael B HoppaDepartment of Biological Sciences, Dartmouth College, Hanover, NH, United States.
Dartmouth College · US

Funding

Understanding the role of RNA-binding protein mutations in cancerP20GM113132 · NIGMS · DARTMOUTH COLLEGE · PI MADDEN, DEAN R · 2016 to 2025
$25.9M
Neuromodulation of cortical circuits in health and diseaseR01MH099054 · NIMH · DARTMOUTH COLLEGE · PI GULLEDGE, ALLAN T · 2013 to 2017
$2.0M
NIGMS NIH HHS P20 GM113132NIMH NIH HHS R01 MH099054
6 · The paper itself

Abstract

The axon initial segment (AIS) is a specialized region within the proximal portion of the axon that initiates action potentials thanks in large part to an enrichment of sodium channels. The scaffolding protein ankyrinG (AnkG) is essential for the recruitment of sodium channels as well as several other intracellular and extracellular proteins to the AIS. In the present study, we explore the role of the cell adhesion molecule (CAM) neurofascin-186 (NF-186) in arranging the individual molecular components of the AIS in cultured rat hippocampal neurons. Using a CRISPR depletion strategy to ablate NF expression, we found that the loss of NF selectively perturbed AnkG accumulation and its relative proximal distribution within the AIS. We found that the overexpression of sodium channels could restore AnkG accumulation, but not its altered distribution within the AIS without NF present. We go on to show that although the loss of NF altered AnkG distribution, sodium channel function within the AIS remained normal. Taken together, these results demonstrate that the regulation of AnkG and sodium channel accumulation within the AIS can occur independently of one another, potentially mediated by other binding partners such as NF.

Indexed as

ankyrin Gaxon initial segmentcultured hippocampal neuronsneurofascin-186voltage gated sodium channels

Identifiers

PMID30723396
PMCPMC6349729
OpenAlexW2913125727

What OpenQuestion holds

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Registered trials

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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.