Evidence map›Paper›PMID 39263607›Full record

ArticleMedComm2024

Loss-of-function variants in RNA binding motif protein X-linked induce neuronal defects contributing to amyotrophic lateral sclerosis pathogenesis.

Di He, Xinyi He, Dongchao Shen, Liyang Liu, Xunzhe Yang, Meng Hao, Yi Wang, Yi Li, Qing Liu, Mingsheng Liu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. The mCells · 2025
    Review
  4. Review
  5. Article
  6. 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

13 authors.

Di HeDepartment of Neurology Beijing Tiantan Hospital, Capital Medical University Beijing China.ORCID https://orcid.org/0000-0002-0755-2348
Xinyi HeState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences and Human Phenome Institute Fudan University Shanghai China.
Dongchao ShenDepartment of Neurology Peking Union Medical College Hospital (PUMCH), Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China.
Liyang LiuMcKusick-Zhang Center for Genetic Medicine, State Key Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College Beijing China.
Xunzhe YangDepartment of Neurology Peking Union Medical College Hospital (PUMCH), Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China.
Meng HaoState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences and Human Phenome Institute Fudan University Shanghai China.
Yi WangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences and Human Phenome Institute Fudan University Shanghai China.
Yi LiState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences and Human Phenome Institute Fudan University Shanghai China.
Qing LiuDepartment of Neurology Peking Union Medical College Hospital (PUMCH), Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China.
Mingsheng LiuDepartment of Neurology Peking Union Medical College Hospital (PUMCH), Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China.
Jiucun WangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences and Human Phenome Institute Fudan University Shanghai China.
Xue ZhangMcKusick-Zhang Center for Genetic Medicine, State Key Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College Beijing China.
Liying CuiDepartment of Neurology Peking Union Medical College Hospital (PUMCH), Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite being one of the most prevalent RNA modifications, the role of N6-methyladenosine (m6A) in amyotrophic lateral sclerosis (ALS) remains ambiguous. In this investigation, we explore the contribution of genetic defects of m6A-related genes to ALS pathogenesis. We scrutinized the mutation landscape of m6A genes through a comprehensive analysis of whole-exome sequencing cohorts, encompassing 508 ALS patients and 1660 population-matched controls. Our findings reveal a noteworthy enrichment of RNA binding motif protein X-linked (

Indexed as

ALSm6A modificationRBMXsingle‐cell sequencingwhole‐exome sequencing

Identifiers

PMID39263607
PMCPMC11387721

What OpenQuestion holds

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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.