ArticleBiochemical and biophysical research communications2012
Induction of REDD1 gene expression in the liver in response to endoplasmic reticulum stress is mediated through a PERK, eIF2α phosphorylation, ATF4-dependent cascade.
Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- A common germline 3' UTR variant controls DDIT4 translation efficiency and stress responses in cancer cells.iScience · 2026Article
- REDD1/DDIT4 counteracts endoplasmic reticulum stress-induced apoptosis by controlling the expression of death receptor TRAILR2/DR5 in cancer cells.Cell death & disease · 2026Article
- REDD1 is a determinant of the sensitivity of renal cell carcinoma cells to autophagy inhibition that can be therapeutically exploited by targeting PIM activity.Cancer letters · 2025Article
- Induction of endoplasmic reticulum stress is associated with the anti-tumor activity of monepantel across cancer types.Cancer medicine · 2023Article
- How autophagy, a potential therapeutic target, regulates intestinal inflammation.Frontiers in immunology · 2023Review
- Article
- ATF4/TXNIP/REDD1/mTOR signaling mediates the antitumor activities of liver X receptor in pancreatic cancers.Cancer innovation · 2022Article
- Protective Effects of Taraxasterol against Deoxynivalenol-Induced Damage to Bovine Mammary Epithelial Cells.Toxins · 2022Article
- Role of Proteasomes in Inflammation.Journal of clinical medicine · 2021Review
- Androgen depletion alters the diurnal patterns to signals that regulate autophagy in the limb skeletal muscle.Molecular and cellular biochemistry · 2021Article
- Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis.Frontiers in pharmacology · 2021Review
- Oral Pathobiont-Induced Changes in Gut Microbiota Aggravate the Pathology of Nonalcoholic Fatty Liver Disease in Mice.Frontiers in immunology · 2021Article
- DDIT4 Novel Mutations in Pancreatic Cancer.Gastroenterology research and practice · 2021Article
- Noise Exposures Causing Hearing Loss Generate Proteotoxic Stress and Activate the Proteostasis Network.Cell reports · 2020Article
- Contribution of the Unfolded Protein Response (UPR) to the Pathogenesis of Proteasome-Associated Autoinflammatory Syndromes (PRAAS).Frontiers in immunology · 2019Review
- Time-resolved analysis of amino acid stress identifies eIF2 phosphorylation as necessary to inhibit mTORC1 activity in liver.The Journal of biological chemistry · 2018Article
- Calcitriol exerts an anti-tumor effect in osteosarcoma by inducing the endoplasmic reticulum stress response.Cancer science · 2017Article
- Time-Course Change of Redd1 Expressions in the Hippocampal CA1 Region Following Chronic Cerebral Hypoperfusion.Cellular and molecular neurobiology · 2017Article
- Is REDD1 a Metabolic Éminence Grise?Trends in endocrinology and metabolism: TEM · 2016Review
- Metformin Treatment Prevents Sedentariness Related Damages in Mice.Journal of diabetes research · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Since the endoplasmic reticulum (ER) plays a vital role in hepatocyte function, it is not surprising that a variety of liver-related diseases are associated with ER stress. As in other tissues, ER stress in the liver leads to generation of the unfolded-protein response resulting in activation of a transcriptional program that promotes restoration of homeostasis within the lumen of the ER. Previous studies using cells in culture demonstrated that ER stress induces expression of REDD1 (regulated in development and DNA damage responses), a potent repressor of signaling through the protein kinase referred to as the mechanistic target of rapamycin in complex 1 (mTORC1). In the present study, the results from the cell culture experiments were extended to show that tunicamycin-mediated ER stress in the liver in vivo also induces REDD1 gene expression. Moreover, the induction of REDD1 gene expression was shown to require the protein kinase PERK and enhanced phosphorylation of its substrate, the α-subunit of eukaryotic initiation factor 2.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.