The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
mTORC1 serves ER stress-triggered apoptosis via selective activation of the IRE1–JNK pathway
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1 retracted
Proapoptotic BAX and BAK Modulate the Unfolded Protein Response by a Direct Interaction with IRE1α
Hetz, C., Bernasconi, P., Fisher, J., Lee, A.-H., Bassik, M. C., Antonsson, B., Brandt, G. S., Iwakoshi, N. N., Schinzel, A., Glimcher, L. H., et al. (2006) · Science · doi:10.1126/science.1123480 · Cited by 667
RetractedA biomarker that identifies senescent human cells in culture and in aging skin in vivo.
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Signal integration in the endoplasmic reticulum unfolded protein response
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AKT/PKB signaling: navigating downstream
Manning, B. D., & Cantley, L. C. (2007) · Cell · doi:10.1016/j.cell.2007.06.009 · Cited by 6,115
TOR signaling in growth and metabolism
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Control of inositol 1,4,5-trisphosphate-induced Ca2+ release by cytosolic Ca2+
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Mutation of the mouse klotho gene leads to a syndrome resembling ageing
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TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling
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Cited by
González-Rodríguez, Á., Mayoral, R., Agra, N., Valdecantos, M. P., Pardo, V, Miquilena-Colina, M. E., Vargas-Castrillón, J., Lo Iacono, O., Corazzari, M., Fimia, G. M., et al. (2014) · Cell Death & Disease · doi:10.1038/cddis.2014.162 · Cited by 615
New insights into ER stress-induced insulin resistance
Flamment, M., Hajduch, E., Ferré, P., & Foufelle, F. (2012) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2012.06.003 · Cited by 306
Metabolic Alterations in Aging Macrophages: Ingredients for Inflammaging?
van Beek, A. A., Van den Bossche, J., Mastroberardino, P. G., de Winther, M. P. J., & Leenen, P. J. M. (2019) · Trends in Immunology · doi:10.1016/j.it.2018.12.007 · Cited by 207
Yasuda, M., Tanaka, Y., Kume, S., Morita, Y., Chin-Kanasaki, M., Araki, H., Isshiki, K., Araki, S.-I., Koya, D., Haneda, M., et al. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2014.04.001 · Cited by 123
“Evidence of crosstalk between mTORC1 and ER stress has recently emerged, as growing research suggests that mTORC1-related ER stress is involved in the pathogenesis of various diabetes-related organ dysfunctions [34,49,54].”
Type I interferons and endoplasmic reticulum stress in health and disease
(2020) · International Review of Cell and Molecular Biology · doi:10.1016/bs.ircmb.2019.10.004 · Cited by 83
Metadata
- Authors
- Kato, H., Nakajima, S., Saito, Y., Takahashi, S., Katoh, R., & Kitamura, M.
- Venue
- Cell Death & Differentiation
- Published
- 2011-07-22
- Volume
- 19
- Issue
- 2
- Pages
- 310-320
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W1991612947
- Cited by
- 272
- References
- 43
- FWCI
- 8.17
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: mTORC1 serves ER stress-triggered apoptosis via selective activation of the IRE1–JNK pathway. https://app.cochat.ai/papers/10.1038/cdd.2011.98
- The paper
- Kato, H., Nakajima, S., Saito, Y., Takahashi, S., Katoh, R., & Kitamura, M. (2012). mTORC1 serves ER stress-triggered apoptosis via selective activation of the IRE1–JNK pathway. Cell Death & Differentiation. https://doi.org/10.1038/cdd.2011.98
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.