Evidence map›Paper›PMID 11464290›Full record

ArticleOncogene2001

Modulation of p53 dependent gene expression and cell death through thioredoxin-thioredoxin reductase by the Interferon-Retinoid combination.

J Hu, X Ma, D J Lindner, S Karra, E R Hofmann, S P Reddy, D V Kalvakolanu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Role of CXCL10 in Spinal Cord Injury.International journal of medical sciences · 2022
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

7 authors at 2 institutions in 1 country.

J HuGreenebaum Cancer Center, Department of Microbiology & Immunology, Molecular and Cellular Biology Program, University of Maryland School of Medicine, Baltimore, Maryland, MD 21201, USA.
X Ma
D J Lindner
S Karra
E R Hofmann
S P Reddy
D V Kalvakolanu
University of Maryland, Baltimore · USJohns Hopkins University · US

Funding

MODULATION OF IFN ACTION VIA NOVEL REGULATORY FACTORSR01CA078282 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI KALVAKOLANU, DHAN V. · 1998 to 2014
$4.4M
TUMOR GROWTH INHIBITION BY INTERFERON B AND RETINOIDSR01CA071401 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI KALVAKOLANU, DHAN V. · 1996 to 2001
$595k
MOLECULAR BASIS OF AIRWAY SQUAMOUS CELL DIFFERENTIATIONR01HL058122 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI POTHIREDDY, SEKHAR M · 2001 to 2002
$234k
MOLECULAR BASIS OF AIRWAY SQUAMOUS CELL DIFFERENTIATIONR29HL058122 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI POTHIREDDY, SEKHAR M · 1998 to 2000
$112k
NCI NIH HHS CA 71401NCI NIH HHS CA 78282NHLBI NIH HHS HL-58122
6 · The paper itself

Abstract

We have shown earlier that the IFN-beta and all-trans retinoic acid (RA) combination, but not the single agents, induces death in several tumor cell lines. Employing a genetic technique we have identified several Genes associated with Retinoid-IFN induced Mortality (GRIM). One of the GRIMs was human thioredoxin reductase (TR), a redox enzyme. Since the overexpressed TR augments IFN/RA stimulated cell death, we explored the mechanisms of TR-mediated death. Here we show that TR augments cell death by upregulating the transcriptional activity of p53 tumor suppressor. This process does not involve a physical increase in levels of p53. Using redox inactive mutants of TR and its substrate, thioredoxin (Trx), we demonstrate that IFN/RA-induced regulation of p53 dependent gene expression requires TR and Trx. In contrast-over-expression of wildtype TR or Trx augment the p53 dependent gene expression in response to IFN/RA treatment. Consistent with these results an increased DNA binding activity of p53 was noted in the presence of TR. These studies identify a novel mechanism of p53 mediated cell death regulation involving redox enzymes.

Indexed as

Bacterial ProteinsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBase SequenceDNA PrimersGene Expression RegulationHumansInterferon-betaThioredoxin-Disulfide ReductaseThioredoxinsTranscription, GeneticTretinoinTumor Cells, CulturedTumor Suppressor Protein p53Bacterial ProteinsDNA PrimersInterferon-betaThioredoxin-Disulfide ReductaseThioredoxinsthioredoxin-thioredoxin reductase hybrid protein, Mycobacterium lepraeTretinoinTumor Suppressor Protein p53

Identifiers

PMID11464290
OpenAlexW2322927147

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.