The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Bidirectional crosstalk between endoplasmic reticulum stress and mTOR signaling
Abstract
Many cellular processes including apoptosis, autophagy, translation, energy metabolism, and inflammation are controlled by the mammalian target of rapamycin (mTOR) kinase and the endoplasmic reticulum (ER) stress pathway, also known as the unfolded protein response (UPR). Although both of these signaling nodes have attracted wide attention in fundamental cell biology and drug discovery, crosstalk between the two pathways has emerged only very recently. mTOR complex 1 (mTORC1) operates both upstream and downstream of ER stress signals, which can either enhance or antagonize the anabolic output of mTORC1. Upon prolonged ER stress, mTORC1 contributes to apoptotic signaling by suppressing the survival kinase Akt through feedback inhibition. Likewise, chronic ER stress obstructs activation of Akt by mTOR complex 2. This review surveys our knowledge of mTOR-ER stress intersections and highlights potential therapeutic implications.
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Cites
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SREBP-regulated lipid metabolism: convergent physiology - divergent pathophysiology
Shimano, H., & Sato, R. (2017) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2017.91 · Cited by 1,174
Endoplasmic reticulum stress signalling-from basic mechanisms to clinical applications
Almanza, A., Carlesso, A., Chintha, C., Creedican, S., Doultsinos, D., Leuzzi, B., Luís, A., McCarthy, N., Montibeller, L., More, S., et al. (2019) · The FEBS Journal · doi:10.1111/febs.14608 · Cited by 1,034
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Self-citationWhere is mTOR and what is it doing there?
Betz, C., & Hall, M. N. (2013) · Journal of Cell Biology · doi:10.1083/jcb.201306041 · Cited by 527
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Metadata
- Authors
- Appenzeller-Herzog, C., & Hall, M. N.
- Venue
- Trends in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2012-05
- Volume
- 22
- Issue
- 5
- Pages
- 274-282
- ISSN
- 0962-8924 (ISSN-L)
- OpenAlex
- W2035863659
- Cited by
- 313
- References
- 24
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- closed
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