Evidence map›Paper›PMID 27308326›Full record

ReviewMolecular & cellular oncology

Mitochondrial death functions of p53.

N D Marchenko, U M Moll

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular & cellular oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

59 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
  3. Ambiguous Role of p53 in Transcription-Dependent Tumor Cell Death.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Review
  6. Transmetalation in Cancer Pharmacology.International journal of molecular sciences · 2025
    Review
  7. Cytotoxic Effect of CuBulletin of experimental biology and medicine · 2025
    Article
  8. Review
  9. Review
  10. Review
  11. ARTS and small-molecule ARTS mimetics upregulate p53 levels by promoting the degradation of XIAP.Apoptosis : an international journal on programmed cell death · 2024
    Article
  12. Article
  13. Review
  14. Characterization of p53/p63/p73 and Myc expressions during embryogenesis of the sea urchin.Developmental dynamics : an official publication of the American Association of Anatomists · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Article
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  20. 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

2 authors at 1 institution in 1 country.

N D MarchenkoDepartment of Pathology; Stony Brook University ; Stony Brook, NY USA.
U M MollDepartment of Pathology; Stony Brook University ; Stony Brook, NY USA.
Stony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 tumor suppressor network plays a fundamental surveillance role in both homeostatic and adaptive cell biology. p53 is one of the most important barriers against malignant derailment of normal cells, orchestrating growth arrest, senescence, or cell death by linking many different pathways in response to genotoxic and non-genotoxic insults. p53 is the key broadband sensor for numerous cellular stresses such as DNA damage, hypoxia, oxidative stress, oncogenic signaling, and nucleolar stress. The crucial tumor suppressive and tissue homeostasis activity of p53 is its ability to activate cell death via multiple different pathways. A well-characterized biochemical function of p53 in the regulation of apoptosis is its role as a potent transcriptional regulator. p53 activates a panel of proapoptotic genes from the mitochondrial apoptotic and death receptor programs while repressing antiapoptotic Bcl2 family genes. In addition, over the last 10 y a growing body of evidence has also defined direct extranuclear non-transcriptional p53 activities within mitochondria-mediated cell death pathways that are based on p53 protein accumulation in cytosolic and mitochondrial compartments and protein-protein interactions. To date, transcription-independent p53-mediated cell death regulation has been described for apoptosis, necrosis, and autophagy. Because mitochondrial dysregulation is central to the development of a number of pathologic processes such as cancer and neurodegenerative and age-related diseases, understanding the direct roles of p53 protein in mitochondria has high translational impact and could facilitate the development of novel drug targets to combat these diseases. In this review we will mainly focus on mechanisms of p53-mediated transcription-independent cell death pathways at mitochondria.

Indexed as

apoptosiscyclophillin Dmitochondrianecrosisp53

Identifiers

PMID27308326
PMCPMC4905191
OpenAlexW1483486462

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.