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REDD1 Is Essential for Optimal T Cell Proliferation and Survival

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. Howeve...

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Detalles Bibliográficos
Autores principales: Reuschel, Emma L., Wang, JiangFang, Shivers, Debra K., Muthumani, Karuppiah, Weiner, David B., Ma, Zhengyu, Finkel, Terri H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547781/
https://www.ncbi.nlm.nih.gov/pubmed/26301899
http://dx.doi.org/10.1371/journal.pone.0136323
Descripción
Sumario: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.