Evidence map›Paper›PMID 17121994›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

The promyelocytic leukemia protein functions as a negative regulator of IFN-gamma signaling.

Youn-Hee Choi, Rosa Bernardi, Pier Paolo Pandolfi, Etty N Benveniste

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

18 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Interaction of promyelocytic leukemia/p53 affects signal transducer and activator of transcription-3 activity in response to oncostatin M.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020
    Article
  4. PML is a ROS sensor activating p53 upon oxidative stress.The Journal of experimental medicine · 2017
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. PML IV/ARF interaction enhances p53 SUMO-1 conjugation, activation, and senescence.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. PML depletion disrupts normal mammary gland development and skews the composition of the mammary luminal cell progenitor pool.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
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 2 institutions in 2 countries.

Youn-Hee ChoiDepartment of Cell Biology, University of Alabama, Birmingham, AL 35294, USA.
Rosa Bernardi
Pier Paolo Pandolfi
Etty N Benveniste
Memorial Sloan Kettering Cancer Center · USUniversity of Alabama at Birmingham · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
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
TRADD as a Regulator of Cytokine Signaling in GliaR01NS050665 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N · 2005 to 2009
$1.6M
NCI NIH HHS P30 CA013148NCI NIH HHS P30 CA 13148NCI NIH HHS R01 CA071692NCI NIH HHS R01 CA 71692NINDS NIH HHS R01 NS050665NINDS NIH HHS R01 NS 50665
6 · The paper itself

Abstract

IFN-gamma is an immunomodulatory cytokine and uses the STAT-1alpha transcription factor to mediate gene expression. The promyelocytic leukemia (PML) protein regulates transcription as an activator or repressor, depending on the gene under investigation. Herein, we examined the influence of PML on IFN-gamma signaling, using PML wild-type (Pml(+/+)) and deficient (Pml(-/-)) mouse embryonic fibroblasts (MEF). Pml(-/-) MEF exhibit enhanced IFN-gamma-induced STAT-1alpha transcriptional activity compared with Pml(+/+) cells. Moreover, reconstitution of PML in Pml(-/-) MEF reduced STAT-1alpha transcriptional activity to levels comparable to Pml(+/+) MEF. Numerous endogenous IFN-gamma-regulated genes were up-regulated in Pml(-/-) MEF compared with Pml(+/+) MEF. IFN-gamma-mediated STAT-1alpha DNA-binding activity was enhanced in Pml(-/-) cells compared with Pml(+/+) cells. Lastly, IFN-gamma enhanced the formation of a PML-STAT-1alpha complex in the nucleus. These data suggest a novel function for PML in the IFN-gamma signaling pathway by inhibiting STAT-1alpha DNA binding and transcriptional activity.

Indexed as

AnimalsCell LineCell Line, TransformedInterferon-gammaMiceNuclear ProteinsPromyelocytic Leukemia ProteinProtein BindingSignal TransductionSTAT1 Transcription FactorTranscription FactorsTumor Suppressor ProteinsInterferon-gammaNuclear ProteinsPml protein, mousePromyelocytic Leukemia ProteinStat1 protein, mouseSTAT1 Transcription FactorTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID17121994
PMCPMC1693728
OpenAlexW1985790922

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.