Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities

Ssang Goo Cho, Jin Woo Kim, Yong Hee Lee, Hyun Sub Hwang, Mi Sung Kim, Kanghyun Ryoo, Myung Jin Kim, Kyung Tae Noh, Eun Kyung Kim, Jun Ho Cho, Kyoung Wan Yoon, Eun Gyung Cho, Hee Sae Park, Sung Wook Chi, Min Jae Lee, Sang Sun Kang, Hidenori Ichijo, Eui Ju Choi

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

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 H2O 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.

Original languageEnglish
Pages (from-to)71-81
Number of pages11
JournalJournal of Cell Biology
Volume163
Issue number1
DOIs
Publication statusPublished - 2003 Oct 13

Fingerprint

MAP Kinase Kinase Kinase 5
Proteins
Apoptosis
caspase-activated DNase inhibitor
caspase-activated deoxyribonuclease
Antisense Oligonucleotides
DNA Fragmentation
Caspase 3
Tumor Necrosis Factor-alpha

Keywords

  • Apoptosis
  • Apoptosis signal-regulating kinase 1
  • C-Jun NH-terminal kinase
  • Caspase-activated DNase
  • Stress-activated protein kinase

ASJC Scopus subject areas

  • Cell Biology

Cite this

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.

In: Journal of Cell Biology, Vol. 163, No. 1, 13.10.2003, p. 71-81.

Research output: Contribution to journalArticle

Cho, SG, Kim, JW, Lee, YH, Hwang, HS, Kim, MS, Ryoo, K, Kim, MJ, Noh, KT, Kim, EK, Cho, JH, Yoon, KW, Cho, EG, Park, HS, Chi, SW, Lee, MJ, Kang, SS, Ichijo, H & Choi, EJ 2003, 'Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities', Journal of Cell Biology, vol. 163, no. 1, pp. 71-81. https://doi.org/10.1083/jcb.200303003
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. In: Journal of Cell Biology. 2003 ; Vol. 163, No. 1. pp. 71-81.
@article{a4c72a7dd2ce4cc58746fe6d3b34d23b,
title = "Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities",
abstract = "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 H2O 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.",
keywords = "Apoptosis, Apoptosis signal-regulating kinase 1, C-Jun NH-terminal kinase, Caspase-activated DNase, Stress-activated protein kinase",
author = "Cho, {Ssang Goo} and Kim, {Jin Woo} and Lee, {Yong Hee} and Hwang, {Hyun Sub} and Kim, {Mi Sung} and Kanghyun Ryoo and Kim, {Myung Jin} and Noh, {Kyung Tae} and Kim, {Eun Kyung} and Cho, {Jun Ho} and Yoon, {Kyoung Wan} and Cho, {Eun Gyung} and Park, {Hee Sae} and Chi, {Sung Wook} and Lee, {Min Jae} and Kang, {Sang Sun} and Hidenori Ichijo and Choi, {Eui Ju}",
year = "2003",
month = "10",
day = "13",
doi = "10.1083/jcb.200303003",
language = "English",
volume = "163",
pages = "71--81",
journal = "Journal of Cell Biology",
issn = "0021-9525",
publisher = "Rockefeller University Press",
number = "1",

}

TY - JOUR

T1 - Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities

AU - Cho, Ssang Goo

AU - Kim, Jin Woo

AU - Lee, Yong Hee

AU - Hwang, Hyun Sub

AU - Kim, Mi Sung

AU - Ryoo, Kanghyun

AU - Kim, Myung Jin

AU - Noh, Kyung Tae

AU - Kim, Eun Kyung

AU - Cho, Jun Ho

AU - Yoon, Kyoung Wan

AU - Cho, Eun Gyung

AU - Park, Hee Sae

AU - Chi, Sung Wook

AU - Lee, Min Jae

AU - Kang, Sang Sun

AU - Ichijo, Hidenori

AU - Choi, Eui Ju

PY - 2003/10/13

Y1 - 2003/10/13

N2 - 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 H2O 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.

AB - 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 H2O 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.

KW - Apoptosis

KW - Apoptosis signal-regulating kinase 1

KW - C-Jun NH-terminal kinase

KW - Caspase-activated DNase

KW - Stress-activated protein kinase

UR - http://www.scopus.com/inward/record.url?scp=0142027916&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0142027916&partnerID=8YFLogxK

U2 - 10.1083/jcb.200303003

DO - 10.1083/jcb.200303003

M3 - Article

C2 - 14557248

AN - SCOPUS:0142027916

VL - 163

SP - 71

EP - 81

JO - Journal of Cell Biology

JF - Journal of Cell Biology

SN - 0021-9525

IS - 1

ER -