Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress

To analyze mechanisms of action of glucocorticoid treatment for endoplasmic reticulum stress (ERS) in sensorineural hearing loss (SNHL), we aimed to evaluate the expression and activation status of the protein kinase RNA-like ER kinase (PERK)–C/EBP homologous protein (CHOP) pathway, which is the maj...

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Autores principales:	Liu Zhibiao, Fei Bing, Xie Lisheng, Liu Jin, Chen Xiaorui, Zhu Wenyan, Lv Lingyun, Ma Wei, Gao Ziwen, Hou Jie, She Wandong
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	endoplasmic reticulum stress perk–chop pathway dexamethasone mifepristone Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/eba06e7f7ce149bc9839bf9fc165fc95
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

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spelling	oai:doaj.org-article:eba06e7f7ce149bc9839bf9fc165fc952021-12-05T14:10:41ZGlucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress2391-541210.1515/biol-2021-0057https://doaj.org/article/eba06e7f7ce149bc9839bf9fc165fc952021-07-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0057https://doaj.org/toc/2391-5412To analyze mechanisms of action of glucocorticoid treatment for endoplasmic reticulum stress (ERS) in sensorineural hearing loss (SNHL), we aimed to evaluate the expression and activation status of the protein kinase RNA-like ER kinase (PERK)–C/EBP homologous protein (CHOP) pathway, which is the major pathway in the ERS.Liu ZhibiaoFei BingXie LishengLiu JinChen XiaoruiZhu WenyanLv LingyunMa WeiGao ZiwenHou JieShe WandongDe Gruyterarticleendoplasmic reticulum stressperk–chop pathwaydexamethasonemifepristoneBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 695-702 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	endoplasmic reticulum stress perk–chop pathway dexamethasone mifepristone Biology (General) QH301-705.5
spellingShingle	endoplasmic reticulum stress perk–chop pathway dexamethasone mifepristone Biology (General) QH301-705.5 Liu Zhibiao Fei Bing Xie Lisheng Liu Jin Chen Xiaorui Zhu Wenyan Lv Lingyun Ma Wei Gao Ziwen Hou Jie She Wandong Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
description	To analyze mechanisms of action of glucocorticoid treatment for endoplasmic reticulum stress (ERS) in sensorineural hearing loss (SNHL), we aimed to evaluate the expression and activation status of the protein kinase RNA-like ER kinase (PERK)–C/EBP homologous protein (CHOP) pathway, which is the major pathway in the ERS.
format	article
author	Liu Zhibiao Fei Bing Xie Lisheng Liu Jin Chen Xiaorui Zhu Wenyan Lv Lingyun Ma Wei Gao Ziwen Hou Jie She Wandong
author_facet	Liu Zhibiao Fei Bing Xie Lisheng Liu Jin Chen Xiaorui Zhu Wenyan Lv Lingyun Ma Wei Gao Ziwen Hou Jie She Wandong
author_sort	Liu Zhibiao
title	Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
title_short	Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
title_full	Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
title_fullStr	Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
title_full_unstemmed	Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
title_sort	glucocorticoids protect hei-oc1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/eba06e7f7ce149bc9839bf9fc165fc95
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Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress

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