Evidence map›Paper›PMID 36004759›Full record

ArticleThe EMBO journal2022

Impaired disassembly of the axon initial segment restricts mitochondrial entry into damaged axons.

Sumiko Kiryu-Seo, Reika Matsushita, Yoshitaka Tashiro, Takeshi Yoshimura, Yohei Iguchi, Masahisa Katsuno, Ryosuke Takahashi, Hiroshi Kiyama

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  8. Tractometry of Human Visual White Matter Pathways in Health and Disease.Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine · 2024
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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

8 authors at 3 institutions in 2 countries.

Sumiko Kiryu-SeoDepartment of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0001-6213-1258
Reika MatsushitaDepartment of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yoshitaka TashiroDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takeshi YoshimuraDepartment of Child Development and Molecular Brain Science, United Graduate School of Child Development, Osaka University, Osaka, Japan.ORCID 0000-0002-0316-8082
Yohei IguchiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masahisa KatsunoDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0001-9453-9311
Ryosuke TakahashiDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiroshi KiyamaDepartment of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0001-5963-046X
Nagoya University · JPKyoto University · JPBaylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proteasome is essential for cellular responses to various physiological stressors. However, how proteasome function impacts the stress resilience of regenerative damaged motor neurons remains unclear. Here, we develop a unique mouse model using a regulatory element of the activating transcription factor (Atf3) gene to label mitochondria in a damage-induced manner while simultaneously genetically disrupting the proteasome. Using this model, we observed that in injury-induced proteasome-deficient mouse motor neurons, the increase of mitochondrial influx from soma into axons is inhibited because neurons fail to disassemble ankyrin G, an organizer of the axon initial segment (AIS), in a proteasome-dependent manner. Further, these motor neurons exhibit amyotrophic lateral sclerosis (ALS)-like degeneration despite having regenerative potential. Selectively vulnerable motor neurons in SOD1

Indexed as

Amyotrophic Lateral SclerosisAxon Initial SegmentAnimalsAnkyrinsAxonsMiceMice, TransgenicMitochondriaMotor NeuronsNerve RegenerationProteasome Endopeptidase ComplexSuperoxide Dismutase-1AnkyrinsProteasome Endopeptidase ComplexSuperoxide Dismutase-1axonal transportnerve injuryneurodegenerative diseaseorganellestress response

Identifiers

PMID36004759
PMCPMC9574747
OpenAlexW4293089531

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.