The stress-responsive protein REDD1 and its pathophysiological functions.
Ji-Yoon KimYoung-Guen KwonYoung-Myeong KimPublished in: Experimental & molecular medicine (2023)
Regulated in development and DNA damage-response 1 (REDD1) is a stress-induced protein that controls various cellular functions, including metabolism, oxidative stress, autophagy, and cell fate, and contributes to the pathogenesis of metabolic and inflammatory disorders, neurodegeneration, and cancer. REDD1 usually exerts deleterious effects, including tumorigenesis, metabolic inflammation, neurodegeneration, and muscle dystrophy; however, it also exhibits protective functions by regulating multiple intrinsic cell activities through either an mTORC1-dependent or -independent mechanism. REDD1 typically regulates mTORC1 signaling, NF-κB activation, and cellular pro-oxidant or antioxidant activity by interacting with 14-3-3 proteins, IκBα, and thioredoxin-interacting protein or 75 kDa glucose-regulated protein, respectively. The diverse functions of REDD1 depend on cell type, cellular context, interaction partners, and cellular localization (e.g., mitochondria, endomembrane, or cytosol). Therefore, comprehensively understanding the molecular mechanisms and biological roles of REDD1 under pathophysiological conditions is of utmost importance. In this review, based on the published literature, we highlight and discuss the molecular mechanisms underlying the REDD1 expression and its actions, biological functions, and pathophysiological roles.
Keyphrases
- oxidative stress
- stress induced
- protein protein
- binding protein
- signaling pathway
- amino acid
- cell fate
- transcription factor
- dna damage
- randomized controlled trial
- cell proliferation
- ischemia reperfusion injury
- adipose tissue
- single cell
- stem cells
- systematic review
- type diabetes
- hiv infected
- skeletal muscle
- human immunodeficiency virus
- cell therapy
- toll like receptor
- anti inflammatory
- diabetic rats
- small molecule
- immune response
- pi k akt
- heat stress
- hepatitis c virus
- childhood cancer