The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Stress and mTORture signaling
Abstract
The TOR (target of rapamycin) pathway is an evolutionarily conserved signaling module regulating cell growth (accumulation of mass) in response to a variety of environmental cues such as nutrient availability, hypoxia, DNA damage and osmotic stress. Its pivotal role in cellular and organismal homeostasis is reflected in the fact that unrestrained signaling activity in mammals is associated with the occurrence of disease states including inflammation, cancer and diabetes. The existence of TOR homologs in unicellular organisms whose growth is affected by environmental factors, such as temperature, nutrients and osmolarity, suggests an ancient role for the TOR signaling network in the surveillance of stress conditions. Here, we will summarize recent advances in the TOR signaling field with special emphasis on how stress conditions impinge on insulin/insulin-like growth factor signaling/TOR signaling.
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The strategic position of mTORC1 at the nexus of nutrient/stress sensing pathways may contribute to the importance of TOR function in regulating lifespan in invertebrates and mammals.
“At the cellular level, mTORC1 helps to coordinate growth and survival responses induced by alterations in nutrient availability, energy status, growth factor stimuli and exposure to potentially lethal cell stresses27–29; this strategic position at the nexus of nutrient/stress sensing pathways may contribute to the importance of TOR function in regulating lifespan in invertebrates and in mammals as”
From Rapamycin fed late in life extends lifespan in genetically heterogeneous mice (2009) · cites this paper as [28]
mTORC1 helps coordinate growth and survival responses induced by alterations in nutrient availability, energy status, growth factor stimuli, and exposure to cell stresses.
“At the cellular level, mTORC1 helps to coordinate growth and survival responses induced by alterations in nutrient availability, energy status, growth factor stimuli and exposure to potentially lethal cell stresses27–29; this strategic position at the nexus of nutrient/stress sensing pathways may contribute to the importance of TOR function in regulating lifespan in invertebrates and in mammals as”
From Rapamycin fed late in life extends lifespan in genetically heterogeneous mice (2009) · cites this paper as [28]
Rapamycin may extend lifespan in old genetically heterogeneous mice through a combination of anti-neoplastic effects and effects on cellular stress resistance and response to nutrient dynamics.
“Rapamycin may extend lifespan in old genetically heterogeneous mice through a combination of anti-neoplastic effects25,26 and effects on cellular stress resistance and response to nutrient dynamics27–29.”
From Rapamycin fed late in life extends lifespan in genetically heterogeneous mice (2009) · cites this paper as [28]
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mTOR: from growth signal integration to cancer, diabetes and ageing
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Metadata
- Authors
- Reiling, J. H., & Sabatini, D. M.
- Venue
- Oncogene
- Published
- 2006-10-16
- Volume
- 25
- Issue
- 48
- Pages
- 6373-6383
- ISSN
- 0950-9232
- 1476-5594
- Cited by
- 311
- References
- 17
- Language
- en
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.
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