Cited by 107Endoplasmic Reticulum Stress and DiseaseCancer-related Molecular PathwaysPI3K/AKT/mTOR signaling in cancer

The eIF2α Kinases PERK and PKR Activate Glycogen Synthase Kinase 3 to Promote the Proteasomal Degradation of p53

Open access
Baltzis, Dionissios, Pluquet, Olivier, Papadakis, Andreas I., Kazemi, Shirin, Qu, Li-Ke, Koromilas, Antonis E.·2007·Journal of Biological Chemistry

Abstract

Phosphorylation of eukaryotic initiation factor 2alpha (eIF2alpha) is mediated by a family of kinases that respond to various forms of environmental stress. The eIF2alpha kinases are critical for mRNA translation, cell proliferation, and apoptosis. Activation of the tumor suppressor p53 results in cell cycle arrest and apoptosis in response to various types of stress. We previously showed that, unlike the majority of stress responses that stabilize and activate p53, induction of endoplasmic reticulum stress leads to p53 degradation through an Mdm2-dependent mechanism. Here, we demonstrate that the endoplasmic reticulum-resident eIF2alpha kinase PERK mediates the proteasomal degradation of p53 independently of translational control. This role is not specific for PERK, because the eIF2alpha kinase PKR also promotes p53 degradation in response to double-stranded RNA. We further establish that the eIF2alpha kinases induce glycogen synthase kinase 3 to promote the nuclear export and proteasomal degradation of p53. Our findings reveal a novel cross-talk between the eIF2alpha kinases and p53 with implications in cell proliferation and tumorigenesis.

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 · 10.1074/jbc.m704491200

Cites

3 of 3 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?

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

Research works printed but not linked: 4

  1. Kimball, S. R., and Jefferson, L. S. (2000) in Translational Control of Gene Expression (Sonenberg, N., Hershey, J. W. B., and Mathews M. B., eds) pp. 561-579, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY 21.
  2. Ron, D., and Harding, H. P. (2000) in Translational Control of Gene Ex- pression (Sonenberg, N., Hershey, J. W. B., and Mathews, M. B., eds) pp. 547-560, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY
  3. Kaufman, R. J. (2000) in Translational Control of Gene Expression (Sonen- berg, N., Hershey, J. W. B., and Mathews, M. B., eds) pp. 503-527, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY 25.
  4. Saunders, L. R., and Barber, G. N. (2003) FASEB J. 17, 961-983

Cited by

Sorted by citations

Authors
Baltzis, D., Pluquet, O., Papadakis, A. I., Kazemi, S., Qu, L.-K., & Koromilas, A. E.
Affiliations
Jewish General Hospital (CA)
Corresponding author
Koromilas, Antonis E.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2007-10
Volume
282
Issue
43
Pages
31675-31687
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2009536847
Cited by
107
References
3
Citations by year
2025: 3 · 2023: 6 · 2022: 3 · 2021: 5 · 2020: 4 · 2019: 5 · 2018: 4 · 2017: 7 · 2016: 3 · 2015: 5 · 2014: 4 · 2013: 8 · 2012: 10
FWCI
4.00
Type
journal article
Language
en
Open access
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • McGill University
  • Terry Fox Foundation
  • National Cancer Institute
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
eIF2α kinase, PERK, PKR, p53 degradation, glycogen synthase kinase-3, endoplasmic reticulum stress, double-stranded RNA, proteasomal degradation, translational regulation, stress response, carcinogenesis
MeSH terms
Animals, Enzyme Activation, Fibrosarcoma, Humans, Models, Biological, RNA, Messenger, Tumor Suppressor Protein p53, eIF-2 Kinase, Glycogen Synthase Kinase 3, NIH 3T3 Cells, Cell Line, Tumor, Proteasome Endopeptidase Complex, 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