Evidence map›Paper›PMID 15626733›Full record

ArticleBlood2005

The promyelocytic leukemia protein PML regulates c-Jun function in response to DNA damage.

Paolo Salomoni, Rosa Bernardi, Stephan Bergmann, Austin Changou, Sara Tuttle, Pier Paolo Pandolfi

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. The PML hub: An emerging actor of leukemia therapies.The Journal of experimental medicine · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Global discovery of high-NaCl-induced changes of protein phosphorylation.American journal of physiology. Cell physiology · 2014
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

6 authors at 1 institution in 1 country.

Paolo SalomoniMemorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, NY, USA.
Rosa Bernardi
Stephan Bergmann
Austin Changou
Sara Tuttle
Pier Paolo Pandolfi
Cornell University · US

Funding

X-RAR alpha proteins: Molecualr Pathogenesis of Acute Promyelocytic LeukemiaR37CA071692 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI PANDOLFI, PIER PAOLO · 2006 to 2010
$1.8M
PML, PLZF, NPM AND NUMA IN THE PATHOGENESIS OF APLR01CA071692 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 1996 to 2005
$1.8M
NCI NIH HHS CA-71692PHS HHS T32
6 · The paper itself

Abstract

The promyelocytic leukemia (PML) gene, a tumor suppressor inactivated in acute promyelocytic leukemia (APL), regulates apoptosis induced by DNA damage. However, the molecular mechanisms by which PML modulates apoptosis following genotoxic stress are only partially elucidated. PML is essential for p53-dependent induction of programmed cell death upon gamma-irradiation through PML-nuclear body (NB)-mediated control of p53 acetylation. Here, we show that PML selectively regulates proapoptotic transcription factors upon different types of DNA damage. We find that Pml inactivation protects fibroblasts from UV-induced apoptosis in a p53-independent manner. We demonstrate that c-Jun is required for UV-induced apoptosis and that PML is essential for both c-Jun transcriptional activation and DNA binding upon UV radiation. We find that PML physically interacts with c-Jun and that upon UV radiation the PML-NBs reorganize into novel nuclear microspeckled structures (UV-NBs), where PML and c-Jun dynamically accumulate. These data identify a novel PML-dependent pathway for c-Jun transcriptional activation and induction of apoptosis in response to DNA damage and shed new light on the role of PML in tumor suppression.

Indexed as

DNA DamageAnimalsApoptosisCells, CulturedEmbryo, MammalianMiceMice, KnockoutNeoplasm ProteinsNuclear ProteinsPromyelocytic Leukemia ProteinProtein BindingProto-Oncogene Proteins c-junTranscriptional ActivationTranscription FactorsTransfectionTumor Suppressor Protein p53Neoplasm ProteinsNuclear ProteinsPml protein, mousePromyelocytic Leukemia ProteinProto-Oncogene Proteins c-junTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID15626733
PMCPMC1895009
OpenAlexW2087789491

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.