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Bis is Induced by Oxidative Stress via Activation of HSF1
The Bis protein is known to be involved in a variety of cellular processes including apoptosis, migration, autophagy as well as protein quality control. Bis expression is induced in response to a number of types of stress, such as heat shock or a proteasome inhibitor via the activation of heat shock...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Physiological Society and The Korean Society of Pharmacology
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211124/ https://www.ncbi.nlm.nih.gov/pubmed/25352760 http://dx.doi.org/10.4196/kjpp.2014.18.5.403 |
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author | Yoo, Hyung Jae Im, Chang-Nim Youn, Dong-Ye Yun, Hye Hyeon Lee, Jeong-Hwa |
author_facet | Yoo, Hyung Jae Im, Chang-Nim Youn, Dong-Ye Yun, Hye Hyeon Lee, Jeong-Hwa |
author_sort | Yoo, Hyung Jae |
collection | PubMed |
description | The Bis protein is known to be involved in a variety of cellular processes including apoptosis, migration, autophagy as well as protein quality control. Bis expression is induced in response to a number of types of stress, such as heat shock or a proteasome inhibitor via the activation of heat shock factor (HSF)1. We report herein that Bis expression is increased at the transcriptional level in HK-2 kidney tubular cells and A172 glioma cells by exposure to oxidative stress such as H(2)O(2) treatment and oxygen-glucose deprivation, respectively. The pretreatment of HK-2 cells with N-acetyl cysteine, suppressed Bis induction. Furthermore, HSF1 silencing attenuated Bis expression that was induced by H(2)O(2), accompaniedby increase in reactive oxygen species (ROS) accumulation. Using a series of deletion constructs of the bis gene promoter, two putative heat shock elements located in the proximal region of the bis gene promoter were found to be essential for the constitutive expression is as well as the inducible expression of Bis. Taken together, our results indicate that oxidative stress induces Bis expression at the transcriptional levels via activation of HSF1, which might confer an expansion of antioxidant capacity against pro-oxidant milieu. However, the possible role of the other cis-element in the induction of Bis remains to be determined. |
format | Online Article Text |
id | pubmed-4211124 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | The Korean Physiological Society and The Korean Society of Pharmacology |
record_format | MEDLINE/PubMed |
spelling | pubmed-42111242014-10-28 Bis is Induced by Oxidative Stress via Activation of HSF1 Yoo, Hyung Jae Im, Chang-Nim Youn, Dong-Ye Yun, Hye Hyeon Lee, Jeong-Hwa Korean J Physiol Pharmacol Original Article The Bis protein is known to be involved in a variety of cellular processes including apoptosis, migration, autophagy as well as protein quality control. Bis expression is induced in response to a number of types of stress, such as heat shock or a proteasome inhibitor via the activation of heat shock factor (HSF)1. We report herein that Bis expression is increased at the transcriptional level in HK-2 kidney tubular cells and A172 glioma cells by exposure to oxidative stress such as H(2)O(2) treatment and oxygen-glucose deprivation, respectively. The pretreatment of HK-2 cells with N-acetyl cysteine, suppressed Bis induction. Furthermore, HSF1 silencing attenuated Bis expression that was induced by H(2)O(2), accompaniedby increase in reactive oxygen species (ROS) accumulation. Using a series of deletion constructs of the bis gene promoter, two putative heat shock elements located in the proximal region of the bis gene promoter were found to be essential for the constitutive expression is as well as the inducible expression of Bis. Taken together, our results indicate that oxidative stress induces Bis expression at the transcriptional levels via activation of HSF1, which might confer an expansion of antioxidant capacity against pro-oxidant milieu. However, the possible role of the other cis-element in the induction of Bis remains to be determined. The Korean Physiological Society and The Korean Society of Pharmacology 2014-10 2014-10-17 /pmc/articles/PMC4211124/ /pubmed/25352760 http://dx.doi.org/10.4196/kjpp.2014.18.5.403 Text en Copyright © 2014 The Korean Physiological Society and The Korean Society of Pharmacology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Yoo, Hyung Jae Im, Chang-Nim Youn, Dong-Ye Yun, Hye Hyeon Lee, Jeong-Hwa Bis is Induced by Oxidative Stress via Activation of HSF1 |
title | Bis is Induced by Oxidative Stress via Activation of HSF1 |
title_full | Bis is Induced by Oxidative Stress via Activation of HSF1 |
title_fullStr | Bis is Induced by Oxidative Stress via Activation of HSF1 |
title_full_unstemmed | Bis is Induced by Oxidative Stress via Activation of HSF1 |
title_short | Bis is Induced by Oxidative Stress via Activation of HSF1 |
title_sort | bis is induced by oxidative stress via activation of hsf1 |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211124/ https://www.ncbi.nlm.nih.gov/pubmed/25352760 http://dx.doi.org/10.4196/kjpp.2014.18.5.403 |
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