Evidence map›Paper›PMID 34966180›Full record

ArticlePediatric research2022

KIF5C deficiency causes abnormal cortical neuronal migration, dendritic branching, and spine morphology in mice.

Wanxing Li, Tianling Cheng, Xinran Dong, Huiyao Chen, Lin Yang, Zilong Qiu, Wenhao Zhou

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Article in Pediatric research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

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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 2 institutions in 1 country.

Wanxing LiDivision of Neonatology, Children's Hospital of Fudan University, 201102, Shanghai, People's Republic of China.
Tianling ChengInstitute of Pediatrics, Children's Hospital, Institutes for Translational Brain Research, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Fudan University, 200032, Shanghai, People's Republic of China.
Xinran DongCenter for Molecular Medicine of Children's Hospital of Fudan University, 201102, Shanghai, People's Republic of China.
Huiyao ChenCenter for Molecular Medicine of Children's Hospital of Fudan University, 201102, Shanghai, People's Republic of China.
Lin YangKey Laboratory of Birth Defects, Children's Hospital of Fudan University, 201102, Shanghai, People's Republic of China.
Zilong QiuInstitute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Center for Brain Science and Brain-Inspired Intelligence Technology, Chinese Academy of Sciences, 200032, Shanghai, People's Republic of China.
Wenhao ZhouDivision of Neonatology, Children's Hospital of Fudan University, 201102, Shanghai, People's Republic of China. zhouwenhao@fudan.edu.cn.
Children's Hospital of Fudan University · CNCenter for Excellence in Brain Science and Intelligence Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMalformation of cortical development (MCD) includes a variety of developmental disorders that are common causes of neurodevelopmental delay and epilepsy. Most recently, clinical studies found that patients carrying KIF5C mutations present early-onset MCD; however, the underlying mechanisms remain elusive.

methodsKIF5C expression level was examined in mouse primary cortical neurons and human ips-derived forebrain organoids. We studied the cortical neuronal migration, dendritic branching, and dendritic spine growth after knocking down the KIF5C gene by electroporation in vitro and in vivo. Then, we studied the transcriptome differences between the knockdown and control groups through RNA sequencing.

resultsWe observed high KIF5C expression in neurons during the early developmental stage in mice and the human brain. Kif5c deficiency results in disturbed cortical neuronal migration, dendritic, and spine growth. Finally, we found that Kif5c knockdown affected several genes associated with cortical neuronal development in vitro.

conclusionsThese results suggested a critical role for Kif5c in cortical development, providing insights into underlying pathogenic factors of kinesins in MCD. IMPACT: KIF5C mutation-related MCD might be caused by abnormal early cortical neuronal development. Kif5c deficiency led to abnormal cortical neuronal dendritic and spine growth and neuronal migration. Our findings explain how Kif5c deficiency is involved in the aberrant development of cortical neurons and provide a new perspective for the pathology of MCD.

Indexed as

EpilepsyKinesinsAnimalsBrainHumansMiceNeurogenesisNeuronsKIF5C protein, humanKIF5C protein, mouseKinesins

Identifiers

PMID34966180
OpenAlexW4200472032

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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.