ArticleCellular signalling2013
Regulated in DNA damage and development 1 (REDD1) promotes cell survival during serum deprivation by sustaining repression of signaling through the mechanistic target of rapamycin in complex 1 (mTORC1).
Article in Cellular signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 85 citations in OpenAlex.
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- YAP promotes global mRNA translation to fuel oncogenic growth despite starvation.Experimental & molecular medicine · 2024Article
- Activating transcription factor 4 in erythroid development andAnnals of hematology · 2024Review
- Phenformin activates ER stress to promote autophagic cell death via NIBAN1 and DDIT4 in oral squamous cell carcinoma independent of AMPK.International journal of oral science · 2024Article
- Mechanisms driving fasting-induced protection from genotoxic injury in the small intestine.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Sublethal engagement of apoptotic pathways in residual cancer.Trends in cell biology · 2024Review
- Dietary leucine supplementation improves growth performance, metabolic responses of liver via GCN2/ATF4, and insulin signaling pathways in largemouth bass (Micropterus salmoides).Fish physiology and biochemistry · 2024Article
- The stress-responsive protein REDD1 and its pathophysiological functions.Experimental & molecular medicine · 2023Review
- PERK/ATF4-dependent expression of the stress response protein REDD1 promotes proinflammatory cytokine expression in the heart of obese mice.American journal of physiology. Endocrinology and metabolism · 2023Article
- Nitrate increases cisplatin chemosensitivity of oral squamous cell carcinoma via REDD1/AKT signaling pathway.Science China. Life sciences · 2021Article
- Discordant regulation of eIF2 kinase GCN2 and mTORC1 during nutrient stress.Nucleic acids research · 2021Article
- Targeting the Integrated Stress Response in Cancer Therapy.Frontiers in pharmacology · 2021Review
- Therapeutic Targeting of Autophagy in Pancreatic Ductal Adenocarcinoma.Frontiers in pharmacology · 2021Review
- Amino Acid Metabolic Vulnerabilities in Acute and Chronic Myeloid Leukemias.Frontiers in oncology · 2021Review
- Bacterial Manipulation of the Integrated Stress Response: A New Perspective on Infection.Frontiers in microbiology · 2021Review
- Circular RNA Microarray Analyses in Hepatic Ischemia-Reperfusion Injury With Ischemic Preconditioning Prevention.Frontiers in medicine · 2021Article
- ATF4-Mediated Upregulation of REDD1 and Sestrin2 Suppresses mTORC1 Activity during Prolonged Leucine Deprivation.The Journal of nutrition · 2020Article
- Development and validation of a 10-gene prognostic signature for acute myeloid leukaemia.Journal of cellular and molecular medicine · 2020Article
- Peripheral blood transcriptome identifies high-risk benign and malignant breast lesions.PloS one · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Regulated in DNA damage and development 1 (REDD1) functions to repress signaling through the mechanistic target of rapamycin (mTOR) protein kinase in complex 1 (mTORC1) in response to diverse stress conditions. In the present study, we investigated the role of REDD1 in the response of cells to growth cessation induced by serum deprivation. REDD1 expression was induced within 2h of depriving cells of serum, with the induction being mediated through ER stress, as evidenced by activation of PERK, enhanced eIF2α phosphorylation, and ATF4 facilitated transcription of the REDD1 gene. In wild-type cells, signaling through mTORC1 was rapidly (within 30min) repressed in response to serum deprivation and the repression was sustained for at least 10h. In contrast, in REDD1 knockout cells mTORC1 signaling recovered toward the end of the 10h-deprivation period. Interestingly, Akt phosphorylation initially declined in response to serum deprivation and then recovered between 2 and 4h in wild-type but not REDD1 knockout cells. The recovery of mTORC1 signaling and the failure of Akt phosphorylation to do so in the REDD1 knockout cells were accompanied by a dramatic increase in caspase-3 cleavage and cell death, both of which were blocked by rapamycin. Furthermore, overexpression of constitutively active Akt rescued REDD1 knockout cells from serum deprivation induced cell death. Overall, the results implicate REDD1 as a key regulatory checkpoint that coordinates growth signaling inputs to activate pro-survival mechanisms and reduce susceptibility to cell death.
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