HERPUD1 protects against oxidative stress-induced apoptosis through downregulation of the inositol 1,4,5-trisphosphate receptor
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- 作者：Felipe Paredesa ; Valentina Parraa ; Natalia Torrealbaa ; Mario Navarro-Marqueza ; Damian Gaticaa ; Roberto Bravo-Saguaa ; Rodrigo Troncosoa ; b ; Christian Pennanena ; Clara Quirogac ; Mario Chionga ; Christa Caesard ; W. Robert Taylord ; e ; Jordi Molgó ; f ; Alejandra San Martine ; Enrique Jaimovichg ; Sergio Lavanderoa ; g ; h ; slavander@uchile.cl" class="auth_mail" title="E-mail the corresponding author
- 关键词：ActD ; actinomycin D ; Ang II ; angiotensin II ; Cat ; catalase ; CHX ; cycloheximide ; CsA ; cyclosporine A ; Cyt-C ; cytochrome c ; ER ; endoplasmic reticulum ; ERAD ; ER-associated degradation ; ERE ; ER stress ; HERPUD1 ; homocysteine-induced ER protein ; ITPR ; inositol 1 ; 4 ; 5-trisphosphate receptor ; JNK ; c-Jun N-terminal kinase ; MPP+ ; methylphenylpyridinium ; MPTP ; mitochondrial permeability transition pore ; Nox ; NAD(P)H oxidase ; RYR ; ryanodine receptor ; VSMC ; vascular smooth muscle cells ; XeB ; xestospongin B
- 刊名：Free Radical Biology and Medicine
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：90
- 期：Complete
- 页码：206-218
- 全文大小：2733 K
文摘
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Oxidative stress by H2O2 or angiotensin II increased HERPUD1 mRNA and protein levels in HeLa cells.
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HERPUD1 knockdown in HeLa cells increased cytosolic Ca2+ levels upon H2O2 stimulation.
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HERPUD1 knockdown in HeLa cells increased inositol trisphosphate receptor protein levels.
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HERPUD1 knockdown increase HeLa apoptosis through a Ca2+-dependent mechanism.