Growth Control Under Stress: mTOR Regulation through the REDD1-TSC Pathway
Open accessAbstract
Dysregulated signaling by the checkpoint kinase TOR (target of rapamycin) has been linked to numerous human cancers. The tuberous sclerosis tumor suppressors TSC1 and TSC2 form a protein complex that integrates and transmits cellular growth factor and stress signals to negatively regulate TOR activity. Several recent reports have identified the stress response gene REDD1 as an essential regulator of TOR activity through the TSC1/2 complex in both Drosophila and mammalian cells. REDD1 is induced in response both to hypoxia and energy stress, and cells that lack REDD1 exhibit highly defective TOR regulation in response to either of these stress signals. While the precise mechanism of REDD1 function remains to be determined, the finding that REDD1-dependent TOR regulation contributes to cell growth/cell size control in flies and mammals suggests that abnormalities of REDD1-mediated signaling might disrupt energy homeostasis and/or promote tumorigenesis.
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Redd1 is a new stress-induced protein and a negative regulator of mTOR through the TSC1/TSC2 complex.
“Redd1 is a new stress-induced protein and is known as a negative regulator of mTOR through TSC1/TSC2 complex [106–115].”
From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [112]
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- Authors
- Ellisen, L. W.
- Affiliations
- Harvard University (US)
- Corresponding author
- Ellisen, Leif W.
- ORCID
- Ellisen, Leif W.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2005-08-22
- Volume
- 4
- Issue
- 11
- Pages
- 1500-1502
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W2024102254
- Cited by
- 131
- References
- 27
- Citations by year
- 2026: 7 · 2025: 2 · 2024: 4 · 2022: 5 · 2021: 3 · 2020: 5 · 2019: 3 · 2018: 8 · 2017: 9 · 2016: 7 · 2015: 3 · 2014: 6 · 2013: 15 · 2012: 13
- FWCI
- 2.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Cancer Society
- Avon Foundation for Women
- National Cancer Institute (R01CA122589)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Physiology › Tuberous Sclerosis Complex Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Keywords
- REDD1, mTOR, TOR signaling, cell growth regulation, cell size control, hypoxia, energy stress, stress response, energy homeostasis, carcinogenesis, Drosophila
- MeSH terms
- Tuberous Sclerosis Complex 1 Protein, Tuberous Sclerosis Complex 2 Protein, Animals, Cell Transformation, Neoplastic, Humans, Protein Kinases, Transcription Factors, Signal Transduction, Oxidative Stress, Tumor Suppressor Proteins, TOR Serine-Threonine Kinases
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