Evidence map›Paper›PMID 38954254›Full record

ArticleMolecular neurobiology2025

BI1 Activates Autophagy and Mediates TDP43 to Regulate ALS Pathogenesis.

Yu Wang, Yuxiang Wang, Hanlan Yin, Zixuan Xiao, Zhichao Ren, Xueting Ma, Jingtian Zhang, Xueqi Fu, Fuqiang Zhang, Linlin Zeng

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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.

Yu Wang *Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China.
Yuxiang Wang *Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China.
Hanlan YinKey Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China.
Zixuan XiaoKey Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China.
Zhichao RenKey Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China.
Xueting MaKey Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China.
Jingtian ZhangCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, Jilin, 130118, China.
Xueqi FuKey Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China.
Fuqiang Zhang *Scientific Research Centre of China-Japan Union Hospital, Jilin University, Changchun, 130033, China. zfqzhang@jlu.edu.cn.
Linlin Zeng *Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China. zenglinlin@jlu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is the most prevalent motor neuron disease in adults. Currently, there are no known drugs or clinical approaches that have demonstrated efficacy in treating ALS. Mitochondrial function and autophagy have been identified as crucial mechanisms in the development of ALS. While Bax inhibitor 1 (BI1) has been implicated in neurodegenerative diseases, its exact mechanism remains unknown. This study investigates the therapeutic impact of BI1 overexpression on ALS both in vivo and in vitro, revealing its ability to mitigate SOD1

Indexed as

Amyotrophic Lateral SclerosisAutophagyDNA-Binding ProteinsMice, TransgenicMotor NeuronsAnimalsApoptosisApoptosis Regulatory ProteinsHumansMiceMitochondriaNeuromuscular JunctionApoptosis Regulatory ProteinsDNA-Binding ProteinsTardbp protein, mouseALSApoptosisExosomeMAMMitochondriaNeurodegenerative disease

Identifiers

What OpenQuestion holds

Textmetadata
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.