Cited by 1,832Endoplasmic Reticulum Stress and DiseaseAutophagy in Disease and TherapyCellular transport and secretion

Autophagy Is Activated for Cell Survival after Endoplasmic ReticulumStress

Open access
Ogata, Maiko, Hino, Shin-ichiro, Saito, Atsushi, Morikawa, Keisuke, Kondo, Shinichi, Kanemoto, Soshi, Murakami, Tomohiko, Taniguchi, Manabu +6 more·2006·Molecular and Cellular Biology

Abstract

Eukaryotic cells deal with accumulation of unfolded proteins in the endoplasmic reticulum (ER) by the unfolded protein response, involving the induction of molecular chaperones, translational attenuation, and ER-associated degradation, to prevent cell death. Here, we found that the autophagy system is activated as a novel signaling pathway in response to ER stress. Treatment of SK-N-SH neuroblastoma cells with ER stressors markedly induced the formation of autophagosomes, which were recognized at the ultrastructural level. The formation of green fluorescent protein (GFP)-LC3-labeled structures (GFP-LC3 "dots"), representing autophagosomes, was extensively induced in cells exposed to ER stress with conversion from LC3-I to LC3-II. In IRE1-deficient cells or cells treated with c-Jun N-terminal kinase (JNK) inhibitor, the autophagy induced by ER stress was inhibited, indicating that the IRE1-JNK pathway is required for autophagy activation after ER stress. In contrast, PERK-deficient cells and ATF6 knockdown cells showed that autophagy was induced after ER stress in a manner similar to the wild-type cells. Disturbance of autophagy rendered cells vulnerable to ER stress, suggesting that autophagy plays important roles in cell survival after ER stress.

Integrity signals

Registry

Crossref · 10.1128/mcb.01453-06

Cites

48 of 48 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Ogata, M., Hino, S.-I., Saito, A., Morikawa, K., Kondo, S., Kanemoto, S., Murakami, T., Taniguchi, M., Tanii, I., Yoshinaga, K., Shiosaka, S., Hammarback, J. A., Urano, F., & Imaizumi, K.
Affiliations
  • University of Miyazaki (JP)
  • Nara Institute of Science and Technology (JP)
  • The University of Osaka (JP)
  • Wake Forest University Health Sciences (US)
  • University of Massachusetts Chan Medical School (US)
Venue
Molecular and Cellular Biology
Published
2006-12-01
Volume
26
Issue
24
Pages
9220-9231
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
OpenAlex
W2127916470
Cited by
1,832
References
48
Citations by year
2026: 27 · 2025: 36 · 2024: 48 · 2023: 86 · 2022: 87 · 2021: 91 · 2020: 115 · 2019: 121 · 2018: 111 · 2017: 121 · 2016: 112 · 2015: 143 · 2014: 143 · 2013: 129 · 2012: 118
FWCI
21.94
Type
journal article
Language
en
Open access
Locations
  • Molecular and Cellular Biology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • eScholarship@UMassChan (submittedVersion)
  • Institutional Repositories DataBase (IRDB) (submittedVersion)
Funders
  • Novartis Foundation
  • Mitsui Sumitomo Insurance Welfare Foundation
  • NOVARTIS Foundation (Japan) for the Promotion of Science
  • Japan Society for the Promotion of Science (17200026)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
Keywords
autophagy, endoplasmic reticulum stress, unfolded protein response, cell survival, IRE1, JNK, PERK, ATF6, LC3, autophagosome formation, neuroblastoma cells, ER-associated degradation, translational attenuation
MeSH terms
Autophagy, Cell Survival, Endoplasmic Reticulum, Enzyme Activation, Humans, Stress, Physiological, Time Factors, Signal Transduction, Protein Folding, Cell Line, Tumor, JNK Mitogen-Activated Protein Kinases

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