Evidence map›Paper›PMID 17173073›Full record

ArticleOncogene2007

Overload of the heat-shock protein H11/HspB8 triggers melanoma cell apoptosis through activation of transforming growth factor-beta-activated kinase 1.

B Li, C C Smith, J M Laing, M D Gober, L Liu, L Aurelian

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Melatonin/Sericin Wound Healing Patches: Implications for Melanoma Therapy.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. GABAPsychopharmacology · 2019
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. High-throughput ectopic expression screen for tamoxifen resistance identifies an atypical kinase that blocks autophagy.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  17. 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

6 authors at 1 institution in 1 country.

B LiDepartment of Pharmacology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
C C Smith
J M Laing
M D Gober
L Liu
L Aurelian
University of Maryland, Baltimore · US

Funding

Training in Molecular and Mechanistic ToxicologyT32ES007263 · NIEHS · UNIVERSITY OF MARYLAND BALTIMORE · PI ALBUQUERQUE, EDSON X · 1990 to 2012
$2.4M
Apoptosis of skin melanoma by the new Hsp H11R01AR053512 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI AURELIAN, LAURE · 2007 to 2011
$1.6M
MOLECULAR STUDIES OF ERYTHEMA MULTIFORMER01AR042647 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI AURELIAN, LAURE · 1994 to 2004
$1.3M
NIAMS NIH HHS AR42647NIAMS NIH HHS R01 AR042647NIAMS NIH HHS R01 AR053512NIEHS NIH HHS ES07263NIEHS NIH HHS T32 ES007263
6 · The paper itself

Abstract

Molecular therapeutics is a recognized promising approach for melanoma, but relevant target genes remain elusive. We report that overload of the recently cloned H11/HspB8 induces apoptosis in 55% of examined melanoma cultures. Apoptosis was determined by activation of caspases-9 and -3 and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL), and was not seen in normal melanocytes. It was associated with H11/HspB8 complexation with transforming growth factor-beta-activated kinase (TAK) 1 and activation of TAK1 and p38 mitogen activated protein 3 kinases. TAK1 was not bound, nor activated by the H11/HspB8 mutant W51C, which has dominant antiapoptotic activity. beta-Catenin was phosphorylated by activated TAK1, inhibiting its nuclear accumulation and mictophthalmia-associated transcription factor and cyclin dependent kinase 2 expression. The dominant-negative TAK1 mutant K63W inhibited beta-catenin phosphorylation and caspase activation. The data indicate that H11/HspB8 overload causes melanoma growth arrest and apoptosis through TAK1 activation and suggest that H11/HspB8 is a promising molecular therapy target.

Indexed as

Apoptosisbeta CateninCaspasesCell NucleusCyclin-Dependent Kinase 2DoxorubicinEnzyme ActivationHeat-Shock ProteinsHumansMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMelanocytesMelanomaMicrophthalmia-Associated Transcription FactorMolecular Chaperonesp38 Mitogen-Activated Protein Kinasesbeta CateninCaspasesCDK2 protein, humanCyclin-Dependent Kinase 2DoxorubicinHeat-Shock ProteinsHSPB8 protein, humanMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMicrophthalmia-Associated Transcription FactorMITF protein, humanMolecular Chaperonesp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine Kinases

Identifiers

PMID17173073
PMCPMC2643355
OpenAlexW2025918958

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.