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Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities
Diverse stimuli initiate the activation of apoptotic signaling pathways that often causes nuclear DNA fragmentation. Here, we report a new antiapoptotic protein, a caspase-activated DNase (CAD) inhibitor that interacts with ASK1 (CIIA). CIIA, by binding to apoptosis signal-regulating kinase 1 (ASK1)...
Autores principales: | , , , , , , , , , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2003
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2173438/ https://www.ncbi.nlm.nih.gov/pubmed/14557248 http://dx.doi.org/10.1083/jcb.200303003 |
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author | Cho, Ssang-Goo Kim, Jin Woo Lee, Yong Hee Hwang, Hyun Sub Kim, Mi-Sung Ryoo, Kanghyun Kim, Myung Jin Noh, Kyung Tae Kim, Eun Kyung Cho, Jun-Ho Yoon, Kyoung Wan Cho, Eun-Gyung Park, Hee-Sae Chi, Sung Wook Lee, Min-Jae Kang, Sang Sun Ichijo, Hidenori Choi, Eui-Ju |
author_facet | Cho, Ssang-Goo Kim, Jin Woo Lee, Yong Hee Hwang, Hyun Sub Kim, Mi-Sung Ryoo, Kanghyun Kim, Myung Jin Noh, Kyung Tae Kim, Eun Kyung Cho, Jun-Ho Yoon, Kyoung Wan Cho, Eun-Gyung Park, Hee-Sae Chi, Sung Wook Lee, Min-Jae Kang, Sang Sun Ichijo, Hidenori Choi, Eui-Ju |
author_sort | Cho, Ssang-Goo |
collection | PubMed |
description | Diverse stimuli initiate the activation of apoptotic signaling pathways that often causes nuclear DNA fragmentation. Here, we report a new antiapoptotic protein, a caspase-activated DNase (CAD) inhibitor that interacts with ASK1 (CIIA). CIIA, by binding to apoptosis signal-regulating kinase 1 (ASK1), inhibits oligomerization-induced ASK1 activation. CIIA also associates with CAD and inhibits the nuclease activity of CAD without affecting caspase-3–mediated ICAD cleavage. Overexpressed CIIA reduces H(2)O(2)- and tumor necrosis factor-α–induced apoptosis. CIIA antisense oligonucleotides, which abolish expression of endogenous CIIA in murine L929 cells, block the inhibitory effect of CIIA on ASK1 activation, deoxyribonucleic acid fragmentation, and apoptosis. These findings suggest that CIIA is an endogenous antagonist of both ASK1- and CAD-mediated signaling. |
format | Text |
id | pubmed-2173438 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21734382008-05-01 Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities Cho, Ssang-Goo Kim, Jin Woo Lee, Yong Hee Hwang, Hyun Sub Kim, Mi-Sung Ryoo, Kanghyun Kim, Myung Jin Noh, Kyung Tae Kim, Eun Kyung Cho, Jun-Ho Yoon, Kyoung Wan Cho, Eun-Gyung Park, Hee-Sae Chi, Sung Wook Lee, Min-Jae Kang, Sang Sun Ichijo, Hidenori Choi, Eui-Ju J Cell Biol Article Diverse stimuli initiate the activation of apoptotic signaling pathways that often causes nuclear DNA fragmentation. Here, we report a new antiapoptotic protein, a caspase-activated DNase (CAD) inhibitor that interacts with ASK1 (CIIA). CIIA, by binding to apoptosis signal-regulating kinase 1 (ASK1), inhibits oligomerization-induced ASK1 activation. CIIA also associates with CAD and inhibits the nuclease activity of CAD without affecting caspase-3–mediated ICAD cleavage. Overexpressed CIIA reduces H(2)O(2)- and tumor necrosis factor-α–induced apoptosis. CIIA antisense oligonucleotides, which abolish expression of endogenous CIIA in murine L929 cells, block the inhibitory effect of CIIA on ASK1 activation, deoxyribonucleic acid fragmentation, and apoptosis. These findings suggest that CIIA is an endogenous antagonist of both ASK1- and CAD-mediated signaling. The Rockefeller University Press 2003-10-13 /pmc/articles/PMC2173438/ /pubmed/14557248 http://dx.doi.org/10.1083/jcb.200303003 Text en Copyright © 2003, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Cho, Ssang-Goo Kim, Jin Woo Lee, Yong Hee Hwang, Hyun Sub Kim, Mi-Sung Ryoo, Kanghyun Kim, Myung Jin Noh, Kyung Tae Kim, Eun Kyung Cho, Jun-Ho Yoon, Kyoung Wan Cho, Eun-Gyung Park, Hee-Sae Chi, Sung Wook Lee, Min-Jae Kang, Sang Sun Ichijo, Hidenori Choi, Eui-Ju Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities |
title | Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities |
title_full | Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities |
title_fullStr | Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities |
title_full_unstemmed | Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities |
title_short | Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities |
title_sort | identification of a novel antiapoptotic protein that antagonizes ask1 and cad activities |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2173438/ https://www.ncbi.nlm.nih.gov/pubmed/14557248 http://dx.doi.org/10.1083/jcb.200303003 |
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