Evidence map›Paper›PMID 39200158›Full record

ArticleBiomedicines2024

KIF1A, R1457Q, and P1688L Mutations Induce Protein Abnormal Aggregation and Autophagy Impairment in iPSC-Derived Motor Neurons.

Mingri Zhao, Junling Wang, Miao Liu, Yaoyao Xu, Jiali Huang, Yiti Zhang, Jianfeng He, Ao Gu, Mujun Liu, Xionghao Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Astrocyte Enrichment of 3D Cortical Constructs Enhances Brain Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Article
  8. Review
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

10 authors.

Mingri ZhaoMOE Key Lab. of Rare Pediatric Diseases, Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410000, China.ORCID 0000-0002-8260-7935
Junling WangDepartment of Neurology, Xiangya Hospital, Central South University, Changsha 410000, China.
Miao LiuMOE Key Lab. of Rare Pediatric Diseases, Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410000, China.
Yaoyao XuMOE Key Lab. of Rare Pediatric Diseases, Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410000, China.
Jiali HuangMOE Key Lab. of Rare Pediatric Diseases, Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410000, China.
Yiti ZhangMOE Key Lab. of Rare Pediatric Diseases, Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410000, China.ORCID 0000-0002-4245-2879
Jianfeng HeMOE Key Lab. of Rare Pediatric Diseases, Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410000, China.
Ao GuMOE Key Lab. of Rare Pediatric Diseases, Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410000, China.
Mujun LiuDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha 410000, China.ORCID 0000-0002-1558-1448
Xionghao LiuMOE Key Lab. of Rare Pediatric Diseases, Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410000, China.ORCID 0000-0002-2633-7096

Funding

the National Key Research and Development Program of China 2016YFC0905100the Natural Science Foundation of Changsha, China kq2202077the Natural Science Foundation of Hunan Province, China 2021JJ30801the Postgraduate Freedom Explo-ration Project of Central South University CX20230291
6 · The paper itself

Abstract

Mutations in the C-terminal of KIF1A (Kinesin family member 1A) may lead to amyotrophic lateral sclerosis (ALS) through unknown mechanisms that are not yet understood. Using iPSC reprogramming technology and motor neuron differentiation techniques, we generated iPSCs from a healthy donor and two ALS patients with KIF1A mutations (R1457Q and P1688L) and differentiated them into spinal motor neurons (iPSC-MN) to investigate

Indexed as

ALSiPSCKIF1Amotor neuron

Identifiers

PMID39200158
PMCPMC11351720

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.