Evidence map›Paper›PMID 16892086›Full record

ReviewOncogene2006

p53 and Nur77/TR3 - transcription factors that directly target mitochondria for cell death induction.

U M Moll, N Marchenko, X-K Zhang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

114 citing papers in PubMed, 240 citations in OpenAlex.

  1. Article
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  4. Review
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  13. 3-Heptylidene-4,6-Dimethoxy-3Molecules (Basel, Switzerland) · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Ethyl Acetate Fraction ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  18. Review
  19. Reposition of the anti-inflammatory drug diacerein in anSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
  20. Article

54 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

3 authors at 2 institutions in 1 country.

U M MollDepartment of Pathology Stony Brook University, Stony Brook, New York 11794-8691, USA. umoll@notes.cc.sunysb.edu
N Marchenko
X-K Zhang
Stony Brook University · USSanford Burnham Prebys Medical Discovery Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complex apoptotic functions of the p53 tumor suppressor are central to its antineoplastic activity in vivo. Conversely, p53 function is altered or attenuated in one way or another in the majority of human cancers. Besides its well-understood action as a transcriptional regulator of multiple apoptotic genes, p53 also exerts a direct pro-apoptotic role at the mitochondria by engaging in protein-protein interactions with anti- and pro-apoptotic Bcl2 family members, thereby executing the shortest known circuitry of p53 death signaling. Nur77, also known as TR3 or NGFI-B, is a unique transcription factor belonging to the orphan nuclear receptor superfamily. Even more extreme than p53, Nur77 can exert opposing biological activities of survival and death. Its activities are regulated by subcellular distribution, expression levels, protein modification and heterodimerization with retinoid X receptor. In cancer cells, Nur77 functions in the nucleus as an oncogenic survival factor, but becomes a potent killer when certain death stimuli induce its migration to mitochondria, where it binds to Bcl2 and conformationally converts it to a killer that triggers cytochrome c release and apoptosis. This review focuses on their unexpected transcription-independent pro-death programs at mitochondria and highlights the remarkable mechanistic similarities between them. Moreover, an accumulating body of evidence provides ample rationale to further investigate how these mitochondrial p53 and Nur77 pathways could become exploitable targets for new cancer therapeutics.

Indexed as

AnimalsApoptosisbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinCytosolDNA-Binding ProteinsHumansMitochondriaNuclear Receptor Subfamily 4, Group A, Member 1Oxidative StressPhosphorylationReceptors, Cytoplasmic and NuclearReceptors, SteroidTranscription FactorsTranscription, GeneticTumor Suppressor Protein p53bcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinDNA-Binding ProteinsNR4A1 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1Receptors, Cytoplasmic and NuclearReceptors, SteroidTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID16892086
OpenAlexW2023373433

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.