Cited by 60Cancer-related Molecular PathwaysHeat shock proteins researchCell death mechanisms and regulation

Genotoxic stress/p53-induced DNAJB9 inhibits the pro-apoptotic function of p53

Open access
Lee, H J, Kim, J M, Kim, K H, Heo, J I, Kwak, S J, Han, J A·2015·Cell Death & Differentiation

Abstract

DNAJB9 is a recently isolated member of the molecular chaperone gene family, whose precise function is largely unknown. In the present study, we have identified DNAJB9 as an inducible gene of the tumor suppressor p53. DNAJB9 expression was induced by p53 or genotoxic stress in a p53-dependent manner, which was mediated by the Ras/Raf/ERK pathway. In addition, depletion of DNAJB9 by using siRNAs greatly increased genotoxic stress/p53-induced apoptosis, suggesting that DNAJB9 inhibits the pro-apoptotic function of p53. We also found that DNAJB9 physically interacts with p53 through its J domain, through which it inhibits the pro-apoptotic function of p53. Moreover, DNAJB9 colocalized with p53 in both cytoplasm and nucleus under genotoxic conditions. Together, these results demonstrate that DNAJB9 is a downstream target of p53 that belongs to the group of negative feedback regulators of p53.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/cdd.2014.116

Cites

33 of 33 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Quantitative proteomic analysis of protein expression changes conferred by asukamycin treatment in 231MFP cells showed many known p53 transcriptional targets upregulated, including GADD45A, GADD45B, ANKRD1, HMOX1, ATF3, PMAIP1, DDIT4, DNAJB9, and PLK2.

    “quantitative proteomic analysis of protein expression changes conferred by asukamycin treatment in 231MFP cells showed many known p53 transcriptional targets upregulated in expression, including GADD45A, GADD45B, ANKRD1, HMOX1, ATF3, PMAIP1, DDIT4, DNAJB9, and PLK2 (Extended Data Figure 9) 31–37.”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Lee, H. J., Kim, J. M., Kim, K. H., Heo, J. I., Kwak, S. J., & Han, J. A.
Affiliations
  • Kangwon National University (KR)
  • Institute for Systems Biology (US)
  • Hallym University (KR)
  • Dankook University (KR)
Corresponding author
Han, J A
Venue
Cell Death & Differentiation
Published
2014-08-22
Volume
22
Issue
1
Pages
86-95
ISSN
  • 1350-9047 (ISSN-L)
  • 1476-5403
OpenAlex
W2006429697
Cited by
60
References
33
Citations by year
2026: 3 · 2025: 5 · 2024: 4 · 2023: 4 · 2022: 3 · 2021: 13 · 2020: 10 · 2019: 6 · 2017: 5 · 2016: 5 · 2015: 2
FWCI
1.93
Type
journal article
Language
en
Open access
Locations
  • Cell Death and Differentiation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Research Foundation
  • National Research Foundation of Korea
  • Ministry of Education, Science and Technology
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
DNAJB9, p53, genotoxic stress, apoptosis, molecular chaperones, Ras/Raf/ERK pathway, p53 target genes, negative feedback regulation, J-domain, p53 stabilization, tumor suppressor
MeSH terms
Animals, Cell Nucleus, Cytoplasm, DNA Damage, Humans, Membrane Proteins, Protein Binding, Tumor Suppressor Protein p53, Apoptosis, Protein Structure, Tertiary, Mice, Knockout, Molecular Chaperones, MAP Kinase Signaling System, Cell Line, Tumor, HSP40 Heat-Shock Proteins, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review