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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2015
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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 |
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author | Reuschel, Emma L. Wang, JiangFang Shivers, Debra K. Muthumani, Karuppiah Weiner, David B. Ma, Zhengyu Finkel, Terri H. |
author_facet | Reuschel, Emma L. Wang, JiangFang Shivers, Debra K. Muthumani, Karuppiah Weiner, David B. Ma, Zhengyu Finkel, Terri H. |
author_sort | Reuschel, Emma L. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4547781 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-45477812015-09-01 REDD1 Is Essential for Optimal T Cell Proliferation and Survival Reuschel, Emma L. Wang, JiangFang Shivers, Debra K. Muthumani, Karuppiah Weiner, David B. Ma, Zhengyu Finkel, Terri H. PLoS One Research Article 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. Public Library of Science 2015-08-24 /pmc/articles/PMC4547781/ /pubmed/26301899 http://dx.doi.org/10.1371/journal.pone.0136323 Text en © 2015 Reuschel et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Reuschel, Emma L. Wang, JiangFang Shivers, Debra K. Muthumani, Karuppiah Weiner, David B. Ma, Zhengyu Finkel, Terri H. REDD1 Is Essential for Optimal T Cell Proliferation and Survival |
title | REDD1 Is Essential for Optimal T Cell Proliferation and Survival |
title_full | REDD1 Is Essential for Optimal T Cell Proliferation and Survival |
title_fullStr | REDD1 Is Essential for Optimal T Cell Proliferation and Survival |
title_full_unstemmed | REDD1 Is Essential for Optimal T Cell Proliferation and Survival |
title_short | REDD1 Is Essential for Optimal T Cell Proliferation and Survival |
title_sort | redd1 is essential for optimal t cell proliferation and survival |
topic | Research Article |
url | 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 |
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