Evidence map›Paper›PMID 39644980›Full record

ArticleNeurobiology of disease2025

KIF5A regulates axonal repair and time-dependent axonal transport of SFPQ granules and mitochondria in human motor neurons.

Irune Guerra San Juan, Jessie W Brunner, Kevin Eggan, Ruud F Toonen, Matthijs Verhage

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Article in Neurobiology of disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Irune Guerra San JuanDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam and VU Medical Center, Amsterdam, the Netherlands; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA; Department of Human Genetics, Amsterdam University Medical Center, Amsterdam, the Netherlands. Electronic address: i.guerrasanjuan@vu.nl.
Jessie W BrunnerDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam and VU Medical Center, Amsterdam, the Netherlands; Department of Human Genetics, Amsterdam University Medical Center, Amsterdam, the Netherlands.
Kevin EgganDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Ruud F ToonenDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam and VU Medical Center, Amsterdam, the Netherlands; Department of Human Genetics, Amsterdam University Medical Center, Amsterdam, the Netherlands.
Matthijs VerhageDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam and VU Medical Center, Amsterdam, the Netherlands; Department of Human Genetics, Amsterdam University Medical Center, Amsterdam, the Netherlands. Electronic address: m.verhage@cncr.vu.nl.

Funding

C9ORF72 in Motor System Biology and ALSR01NS089742 · NINDS · HARVARD UNIVERSITY · PI EGGAN, KEVIN C · 2014 to 2018
$2.3M
NINDS NIH HHS R01 NS089742
6 · The paper itself

Abstract

Mutations in the microtubule-binding motor protein kinesin 5 A (KIF5A) are implicated in several adult-onset motor neuron diseases, including Amyotrophic Lateral Sclerosis, Spastic Paraplegia Type 10 and Charcot-Marie-Tooth Disease Type 2. While KIF5 family members transport a variety of cargos along axons, the specific cargos affected by KIF5A mutations remain poorly understood. Here, we generated KIF5Anull mutant human motor neurons and analyzed the impact on axonal transport and motor neuron outgrowth and regeneration in vitro. KIF5A deficiency caused reduced neurite complexity in young neurons (DIV14) and defects in axonal regeneration. KIF5A deficiency did not affect neurofilament transport but impaired mitochondrial motility and anterograde speed at DIV42. Notably, KIF5A deficiency strongly reduced anterograde transport of splicing factor proline/glutamine-rich (SFPQ)-associated RNA granules in DIV42 axons. Hence, KIF5A plays a critical role in promoting axonal regrowth after injury and in driving the anterograde transport of mitochondria and especially SFPQ-associated RNA granules in mature neurons.

Indexed as

Axonal TransportAxonsKinesinsMitochondriaMotor NeuronsCells, CulturedHumansNerve RegenerationNeuronal OutgrowthPTB-Associated Splicing FactorKIF5A protein, humanKinesinsPTB-Associated Splicing FactorAgingAxonal injury and repairAxonal transportHuman neuron developmentHuman neuronsKIF5AKinesinsMitochondriaMotor neuronsNeurodegenerationNeurofilamentsRNA granules

Identifiers

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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.