Evidence map›Paper›PMID 36565718›Full record

ReviewJournal of molecular cell biology2023

The ARTS of p53-dependent mitochondrial apoptosis.

Qian Hao, Jiaxiang Chen, Hua Lu, Xiang Zhou

Open access · goldAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
12.7field-weighted citation impact, top 1% of its field
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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Current status of radionuclide therapy targeting PARP in cancer: challenges and prospects.European journal of nuclear medicine and molecular imaging · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Cephaeline promotes ferroptosis in breast cancer via p53/SLC7A11/GPX4 axis.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Molecular Mechanisms of Cadmium-Induced Apoptosis in Fish Cells: A Review.International journal of molecular sciences · 2026
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

21 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Qian HaoFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Jiaxiang ChenDepartment of Physiology, Medical College of Nanchang University, Nanchang 330006, China.
Hua LuDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Xiang ZhouFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Shanghai Medical College of Fudan University · CNNanchang University · CNTulane University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor-suppressive activity of p53 is largely attributed to its ability to induce cell death, including apoptosis, through transcription-dependent and transcription-independent mechanisms. On the one hand, nuclear p53 transcriptionally activates the expression of a myriad of pro-apoptotic BCL-2 family genes, such as NOXA, PUMA, BID, BAD, BIK, BAX, etc., whereas it inactivates the expression of anti-apoptotic BCL-2, BCL-XL, and MCL1, leading to mitochondrial apoptosis. On the other hand, cytoplasmic p53 also promotes mitochondrial apoptosis by directly associating with multiple BCL-2 family proteins in the mitochondria. Apoptosis-related protein in TGF-β signaling pathway (ARTS), a mitochondria-localized pro-apoptotic protein encoded by an alternative spliced variant of the SEPT4 gene, triggers apoptosis by facilitating proteasomal degradation of BCL-2 and XIAP upon pro-apoptotic stimuli. We recently identified SEPT4/ARTS as a new p53 target gene in response to genotoxic stress. ARTS in turn binds to p53, drives its mitochondrial localization, and enhances the interaction between p53 and BCL-XL, thereby promoting mitochondrial apoptosis. This review will illustrate the mechanisms of p53-induced mitochondrial apoptosis, offer some recently discovered new insights into the functions of ARTS in regulating mitochondrial cell death, and discuss the clinical significance of ARTS in cancer and non-cancer diseases.

Indexed as

ApoptosisMitochondriaSeptinsApoptosis Regulatory ProteinsProto-Oncogene Proteins c-bcl-2Tumor Suppressor Protein p53Apoptosis Regulatory ProteinsProto-Oncogene Proteins c-bcl-2SEPTIN4 protein, humanSeptinsTumor Suppressor Protein p53apoptosisARTSBCL-2 familycancer therapyp53SEPT4

Identifiers

PMID36565718
PMCPMC10053023
OpenAlexW4312141169

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.