Evidence map›Paper›PMID 39551802›Full record

ArticleCell death & disease2024

TSG101 depletion dysregulates mitochondria and PML NBs, triggering MAD2-overexpressing interphase cell death (MOID) through AIFM1-PML-DAXX pathway.

Yao Xi, Rui Xu, Shengnan Chen, Jiezhu Fang, Xiang Duan, Yidan Zhang, Guoli Zhong, Zhifei He, Yan Guo, Xinyu Li and 5 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Yao XiNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Rui XuNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Shengnan ChenNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Jiezhu FangNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.ORCID 0009-0004-3307-9891
Xiang DuanNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Yidan ZhangNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Guoli ZhongNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Zhifei HeNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Yan GuoJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210032, China.
Xinyu LiJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210032, China.
Wenzhi TaoNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Yang LiNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Yan LiNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China.
Lei FangJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210032, China. njfanglei@nju.edu.cn.ORCID 0000-0002-2582-4845
Yohei NiikuraNational Resource Center for Mutant Mice, MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Medical School of Nanjing University, Nanjing, 210061, China. niikura@nju.edu.cn.ORCID 0000-0002-0392-313X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31970665National Natural Science Foundation of China (National Science Foundation of China) 32071256National Natural Science Foundation of China (National Science Foundation of China) 82141111
6 · The paper itself

Abstract

Overexpression of mitotic arrest deficiency 2 (MAD2/MAD2L1), a pivotal component of the spindle assembly checkpoint (SAC), resulted in many types of cancer. Here we show that the depletion of tumor susceptibility gene 101 (TSG101), causes synthetic dosage lethality (SDL) in MAD2-overexpressing cells, and we term this cell death MAD2-overexpressing interphase cell death (MOID). The induction of MOID depends on PML and DAXX mediating mitochondrial AIFM1-release. MAD2, TSG101, and AIF-PML-DAXX axis regulate mitochondria, PML nuclear bodies (NBs), and autophagy with close inter-dependent protein stability in survival cells. Loss of C-terminal phosphorylation(s) of TSG101 and closed (C-)MAD2-overexpression contribute to induce MOID. In survival cells, both MAD2 and TSG101 localize at PML NBs in interphase, and TSG101 Y390 phosphorylation is required for localization of TSG101 to PML NBs. PML release from PML NBs through PML deSUMOylation contributes to induce MOID. The post-transcriptional/translational cell death machinery and the non-canonical transcriptional regulation are intricately linked to MOID, and ER-MAM, may serve as a crucial intersection for MOID signaling.

Indexed as

Autophagic Cell DeathGenes, NeoplasmMad2 ProteinsNeoplasmsPromyelocytic Leukemia Nuclear BodiesAnimalsApoptosis Inducing FactorCell DeathCell LineChromosomal InstabilityCo-Repressor ProteinsDNA RepairGene Expression Regulation, NeoplasticHumansIntracellular MembranesMaleAIFM1 protein, humanApoptosis Inducing FactorCo-Repressor ProteinsDAXX protein, humanMad2 ProteinsMolecular ChaperonesReactive Oxygen SpeciesTsg101 Protein

Identifiers

PMID39551802
PMCPMC11570632

What OpenQuestion 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 OpenQuestion graph.