Evidence map›Paper›PMID 38918620›Full record

ArticleCell death and differentiation2024

E3 ubiquitin ligase TRIM31 alleviates dopaminergic neurodegeneration by promoting proteasomal degradation of VDAC1 in Parkinson's Disease model.

Ze Zhao, Xiaomeng Song, Yimeng Wang, Lu Yu, Gan Huang, Yiquan Li, Runzhe Zong, Tengfei Liu, Qiuran Ji, Yi Zheng and 5 more

Abstract read
In one paragraph

Article in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

15 authors.

Ze Zhao *Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Xiaomeng Song *Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Yimeng WangDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Lu YuDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Gan HuangDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Yiquan LiDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Runzhe ZongDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Tengfei LiuDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Qiuran JiDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China.
Yi ZhengKey Laboratory of Infection and Immunity of Shandong Province & Department of Immunology, School of Basic Medical Sciences, Shandong University, Jinan, PR China.ORCID 0000-0001-9579-1711
Bingyu LiuKey Laboratory of Infection and Immunity of Shandong Province & Department of Immunology, School of Basic Medical Sciences, Shandong University, Jinan, PR China.ORCID 0000-0003-4817-5355
Qingfen ZhuShandong Institute for Food and Drug Control, Jinan, Shandong, PR China.
Lin ChenDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China. linchen@sdu.edu.cn.
Chengjiang GaoKey Laboratory of Infection and Immunity of Shandong Province & Department of Immunology, School of Basic Medical Sciences, Shandong University, Jinan, PR China. cgao@sdu.edu.cn.ORCID 0000-0002-9365-4497
Huiqing LiuDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, PR China. liuhuiqing@sdu.edu.cn.ORCID 0000-0001-8866-3957

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81571171National Natural Science Foundation of China (National Science Foundation of China) 81873748National Natural Science Foundation of China (National Science Foundation of China) 81971193
6 · The paper itself

Abstract

Mitochondrial dysfunction plays a pivotal role in the pathogenesis of Parkinson's disease (PD). As a mitochondrial governor, voltage-dependent anion channel 1 (VDAC1) is critical for cell survival and death signals and implicated in neurodegenerative diseases. However, the mechanisms of VDAC1 regulation are poorly understood and the role of tripartite motif-containing protein 31 (TRIM31), an E3 ubiquitin ligase which is enriched in mitochondria, in PD remains unclear. In this study, we found that TRIM31

Indexed as

Disease Models, AnimalDopaminergic NeuronsProteasome Endopeptidase ComplexTripartite Motif ProteinsUbiquitin-Protein LigasesVoltage-Dependent Anion Channel 1AnimalsCell Line, TumorMaleMiceMice, Inbred C57BLMice, KnockoutParkinson DiseaseProteolysisUbiquitinationProteasome Endopeptidase ComplexTRIM31 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesVdac1 protein, mouseVoltage-Dependent Anion Channel 1

Identifiers

PMID38918620
PMCPMC11519394

What Socratic 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 Socratic graph.