title: REDD1 Is Essential for Optimal T Cell Proliferation and Survival.
abstract: REDD1 is a highly conserved stress response protein that is upregulated following many types of cellular stress, including hypoxia, DNA damage, energy stress, ER stress, and nutrient deprivation. Recently, REDD1 was shown to be involved in dexamethasone induced autophagy in murine thymocytes. However, we know little of REDD1's function in mature T cells. Here we show for the first time that REDD1 is upregulated following T cell stimulation with PHA or CD3/CD28 beads. REDD1 knockout T cells exhibit a defect in proliferation and cell survival, although markers of activation appear normal. These findings demonstrate a previously unappreciated role for REDD1 in T cell function.
authors: Division of Rheumatology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America.
authors: Emma L
authors: EL
authors: Reuschel
authors: Division of Rheumatology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America.
authors: JiangFang
authors: J
authors: Wang
authors: Division of Rheumatology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America.
authors: Debra K
authors: DK
authors: Shivers
authors: Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America.
authors: Karuppiah
authors: K
authors: Muthumani
authors: Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America.
authors: David B
authors: DB
authors: Weiner
authors: Division of Rheumatology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America.
authors: Zhengyu
authors: Z
authors: Ma
authors: Division of Rheumatology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America.
authors: Terri H
authors: TH
authors: Finkel
mesh_terms: D000818:Animals; D001343:Autophagy / Q000187:drug effects / Q000235:genetics*; D049109:Cell Proliferation / Q000187:drug effects / Q000235:genetics*; D002470:Cell Survival / Q000235:genetics*; D004249:DNA Damage / Q000235:genetics; D003907:Dexamethasone / Q000008:administration & dosage; D051379:Mice; D018345:Mice, Knockout; D013601:T-Lymphocytes / Q000378:metabolism; D060168:Thymocytes / Q000378:metabolism / Q000473:pathology; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism; D015533:Transcriptional Activation / Q000187:drug effects
chemical_list: C469992:Ddit4 protein, mouse; D014157:Transcription Factors; D003907:Dexamethasone