Identification and characterization of Ich-3, a member of the interleukin-1 beta converting enzyme (ICE)/Ced-3 family and an upstream regulator of ICE

被引：194

作者：

Wang, SY

Miura, M

Jung, YK

Zhu, H

Gagliardini, V

Shi, LF

Greenberg, AH

Yuan, JY

机构：

[1] MASSACHUSETTS GEN HOSP EAST,CARDIOVASC RES CTR,CHARLESTOWN,MA 02129

[2] HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115

[3] UNIV TSUKUBA,DEPT MOL NEUROBIOL,CTR TSUKUBA ADV RES ALLIANCE,TSUKUBA,IBARAKI 305,JAPAN

[4] UNIV TSUKUBA,INST BASIC MED SCI,TSUKUBA,IBARAKI 305,JAPAN

[5] UNIV MANITOBA,MANITOBA INST CELL BIOL,MANITOBA CANC TREATMENT & RES FDN,WINNIPEG,MB R3E 0V9,CANADA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 1996年 / 271卷 / 34期

关键词：

D O I：

10.1074/jbc.271.34.20580

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We report here the isolation and characterization of a new member of the ice/ced-3 family of cell death genes, named ich-3. The predicted amino acid sequence of Ich-3 protein shares 54% identity with murine interleukin-1 beta converting enzyme (ICE). Overexpression of ich-3 in Rat-1 and HeLa cells induces apoptosis, which can be inhibited by CrmA and Bcl-2. The mRNA and proteins of ich-3 are dramatically induced in vivo upon stimulation with lipopolysaccharide, an inducer of septic shock. The ich-3 gene product can be cleaved by cytotoxic T cells granule serine protease granzyme B, suggesting that Ich-3 may mediate apoptosis induced by granzyme B. Ich-3 does not process proIL-1 beta directly but does promote proIL-1 beta processing by ICE. These results suggest that Ich-3 may play a very important role in apoptosis and inflammatory responses and may be an upstream regulator of ICE.

引用

页码：20580 / 20587

页数：8

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