Apop-1 Induces caspase-dependent Apoptosis

被引：0

作者：

Sun, Xin ^{[1
]}

Lv, Gang ^{[1
]}

Gao, Ling ^{[1
]}

Kong, Fanli ^{[1
]}

Zhu, Xiaotao ^{[2
]}

Tian, Dan ^{[1
]}

Tong, Haibin ^{[1
]}

Chu, Xiaodan ^{[1
]}

Xie, Yu

机构：

[1] Beihua Univ China, Life Sci Ctr, Jilin, Jilin, Peoples R China

[2] Cent Hosp Jilin, Dept Surg, Jilin, Jilin, Peoples R China

来源：

2010 4TH INTERNATIONAL CONFERENCE ON BIOINFORMATICS AND BIOMEDICAL ENGINEERING (ICBBE 2010) | 2010年

关键词：

Apop-1; VSMC; Apoptosis; SMOOTH-MUSCLE-CELLS; ATHEROSCLEROTIC PLAQUES; CYTOCHROME-C; MITOCHONDRIA; RELEASE; DEATH;

D O I：

暂无

中图分类号：

R318 [生物医学工程];

学科分类号：

0831 ;

摘要：

Apoptosis is a form of genetically programmed cell death, which plays a pivotal role in normal development and the maintenance of homeostasis of a variety of tissues including cardiovascular system. Apop-1 is a soluble protein consisting of 194 amino acids with a mitochondrial localization signal at its N-terminus. RT-PCR data revealed that Apop-1 is expressed in all the organs tested. Immunofluorescence study showed that Apop-1 protein is localized in mitochondria. Transient transfection experiment showed Apop-1 induces apoptosis of cultured VSMC, and this apoptosis is inhibited by a pan-caspase inhibitor Z-VAD. The apoptosis induced by Apop-1 may contribute to the loss of VSMC in atherosclerosis, which will influence the stability of atherosclerotic plaques.

引用

页数：4

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