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福替林与转化生长因子-β刺激克隆-22(TSC-22)之间的相互作用通过使TSC-22不稳定来防止细胞凋亡。

Interaction between fortilin and transforming growth factor-beta stimulated clone-22 (TSC-22) prevents apoptosis via the destabilization of TSC-22.

作者信息

Lee Jeong Heon, Rho Seung Bae, Park Sang-Yoon, Chun Taehoon

机构信息

Department of Obstetrics and Gynecology, Chonbuk National University Medical School, Jeonju 561-712, Republic of Korea.

出版信息

FEBS Lett. 2008 Apr 9;582(8):1210-8. doi: 10.1016/j.febslet.2008.01.066. Epub 2008 Mar 4.

DOI:10.1016/j.febslet.2008.01.066
PMID:18325344
Abstract

Yeast two-hybrid screening was conducted using a human ovary cDNA library to search for a novel binding protein using transforming growth factor-beta stimulated clone-22 (TSC-22). The selected protein was fortilin, which has been characterized as a nuclear anti-apoptotic protein. Overexpression of fortilin in ovarian carcinoma cells reversed TSC-22-mediated apoptosis, and the inhibition of fortilin expression via small interfering RNA (siRNA) resulted in an increase in the apoptosis of ovarian carcinoma cells. Moreover, fortilin overexpression promoted the degradation of TSC-22. Thus, an interaction between fortilin and TSC-22 prevents apoptosis via the destabilization of TSC-22 in ovarian carcinoma cells.

摘要

利用人卵巢cDNA文库进行酵母双杂交筛选,以寻找与转化生长因子-β刺激克隆-22(TSC-22)结合的新型蛋白。筛选出的蛋白是福替林,它被鉴定为一种核抗凋亡蛋白。在卵巢癌细胞中过表达福替林可逆转TSC-22介导的细胞凋亡,而通过小干扰RNA(siRNA)抑制福替林表达则会导致卵巢癌细胞凋亡增加。此外,福替林过表达促进了TSC-22的降解。因此,福替林与TSC-22之间的相互作用通过破坏卵巢癌细胞中TSC-22的稳定性来阻止细胞凋亡。

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1
Interaction between fortilin and transforming growth factor-beta stimulated clone-22 (TSC-22) prevents apoptosis via the destabilization of TSC-22.福替林与转化生长因子-β刺激克隆-22(TSC-22)之间的相互作用通过使TSC-22不稳定来防止细胞凋亡。
FEBS Lett. 2008 Apr 9;582(8):1210-8. doi: 10.1016/j.febslet.2008.01.066. Epub 2008 Mar 4.
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引用本文的文献

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Transforming Stimulated Clone 22 (TSC-22) Interacts Directly with Bromodomain-Containing Protein 7 (BRD7) to Enhance the Inhibition of Extracellular Signal-Regulate Kinase (ERK) Pathway in Ovarian Cancer.转化刺激克隆22(TSC-22)与含溴结构域蛋白7(BRD7)直接相互作用,以增强对卵巢癌中细胞外信号调节激酶(ERK)通路的抑制作用。
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