Origin, expression and possible functions of the two alternatively spliced forms of the mouse Nedd2 mRNA

被引：28

作者：

Kumar, S ^{[1
]}

Kinoshita, M ^{[1
]}

Dorstyn, L ^{[1
]}

Noda, M ^{[1
]}

机构：

[1] KYOTO UNIV,SCH MED,DEPT MOL ONCOL,KYOTO 606,JAPAN

来源：

CELL DEATH AND DIFFERENTIATION | 1997年 / 4卷 / 05期

基金：

英国惠康基金; 英国医学研究理事会;

关键词：

ICE; CED-3; ICH-1; caspases; apoptosis; protease activation;

D O I：

10.1038/sj.cdd.4400251

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：

The Nedd2 gene, a member of the ICE/ced-3 family, transcribes two mRNA species by differential splicing. One of these encodes a shorter truncated version of the protein termed Nedd2s/ICH-1s. While Nedd2/ICH-1 induces apoptosis, ICH-1s was proposed to be a negative regulator of cell death. In this communication we have analyzed various aspects of the Nedd2s/ICH-1s. The coding region of mouse Nedd2 consists of 10 exons and alternative splicing of the 7th exon results in the generation of two transcripts. Although Nedd2s expression conferred partial resistance to serum withdrawal-induced apoptosis in NIH-3T3 cells, it failed to prevent cell death induced by the overexpression of Nedd2 and was unable to suppress apoptosis in two other cell lines (N18 and FDC-P1) under factor deprived conditions. Our results indicate that Nedd2s/ICH-1s is not a general modulator of cell death.

引用

页码：378 / 387

页数：10

共 43 条

[41] The Caenorhabditis elegans cell-death protein CED-3 is a cysteine protease with substrate specificities similar to those of the human CPP32 protease [J].