Advance in the research of the ubiquitin-like molecule FAT10-文献传递-植物通论文库

摘要：摘要：泛素在20世纪70年代中期被发现，随后与泛素类似的小蛋白家族，称泛素样蛋白(ubiquitin-like proteins， UBLs)被报道，并且新成员不断增加。FAT10(human leukocyte antigen F-associated transcript 10)是泛素样蛋白家族的新成员。当用IFN-g和TNF-a刺激细胞时，IFN-g和TNF呈现强协同作用，诱导FAT10修饰其底物，并通过蛋白酶体促使底物蛋白被快速降解。在细胞周期的前期和中期中，高表达FAT10减少定位在动粒上的MAD2分子，从而增加染色体的不稳定性。此外，FAT10表达可以导致细胞凋亡。FAT10的表达可以被p53调控，并且在肝癌细胞、胃癌细胞和妇科癌中FAT10表达上调。该文综述近几年来关于FAT10蛋白的研究进展。
关键词：FAT10；泛素样蛋白；蛋白酶体；凋亡；癌症

Abstract:After the ubiquitin was found in the middle of the 1970s， the ubiquitin-like protein family (UBLs) was subsequently identified. And the new members continue to increase. FAT10 is a new member of the ubiquitin-like protein family， which can be detected in a wide range of human cell lines when the cells were treated with the cytokines interferon ( IFN-g) and tumor necrosis factor (TNF-a). Interestingly， when using IFN-g and TNF-a stimulated the cells， IFN-g and TNF-a show strong synergy to induce FAT10 modification of its substrates and promote the substrates be rapidly degraded. High expression of FAT10 can decrease the molecules positioning on the kinetochore MAD2 and then increase chromosomal instability in the early and mid-term cell cycle. In addition， FAT10 expression can lead to apoptosis and can be regulated by p53. Also， FAT10 could be upregulated in liver cancer， gastric cancer and gynecological cancer. This review summarizes the advance of the ubiquitin-like molecule (UBL) FAT10 in recent years.
Key words: FAT10；ubiquitin-like modifier；proteasome；apoptosis；cancer

全文：生命科学
Chinese Bulletin of Life Sciences
第22卷第2期
2010年2月
Vol. 22, No. 2
Feb., 2010
文章编号：1004-0374(2010)02-0124-05
收稿日期：2009-06-17；修回日期：2009-10-12
基金项目：国家高技术发展计划(“8 6 3 ”计划)
(2006AA02A310); 国家重点基础研究发展计划(“973”
计划) (2006CB910802); 国家自然科学创新群体基金资
助项目(30621063)
*通讯作者：E-mail：wangjian@nic.bmi.ac.cn
泛素样分子FAT10 研究进展
冷泠，王　建*，贺福初
( 军事医学科学院放射与辐射医学研究所，北京蛋白质组研究中心，蛋白质组学国家重点实验室，北京 102206)
摘要：泛素在20世纪70年代中期被发现，随后与泛素类似的小蛋白家族，称泛素样蛋白(ubiquitin-like
proteins， UBLs)被报道，并且新成员不断增加。FAT10(human leukocyte antigen F-associated transcript
10)是泛素样蛋白家族的新成员。当用IFN-γ和 TNF-α刺激细胞时，IFN-γ和 TNF 呈现强协同作用，诱
导 FAT10 修饰其底物，并通过蛋白酶体促使底物蛋白被快速降解。在细胞周期的前期和中期中，高表
达 FA T 1 0 减少定位在动粒上的 MA D 2 分子，从而增加染色体的不稳定性。此外，FA T 1 0 表达可以导
致细胞凋亡。FAT10 的表达可以被 p53 调控，并且在肝癌细胞、胃癌细胞和妇科癌中 FAT10 表达上调。
该文综述近几年来关于 FAT10 蛋白的研究进展。
关键词：F A T 1 0 ；泛素样蛋白；蛋白酶体；凋亡；癌症
中图分类号：Q51; R730.23　　文献标识码：A
Advance in the research of the ubiquitin-like molecule FAT10
LENG Ling, WANG Jian*, HE Fu-chu
(State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine,
Beijing 102206, China)
Abstract: After the ubiquitin was found in the middle of the 1970s, the ubiquitin-like protein family (UBLs) was
subsequently identified. And the new members continue to increase. FAT10 is a new member of the ubiquitin-
like protein family, which can be detected in a wide range of human cell lines when the cells were treated with the
cytokines interferon ( IFN-γ) and tumor necrosis factor (TNF-α). Interestingly, when using IFN-γ and TNF-α
stimulated the cells, IFN-γ and TNF-α show strong synergy to induce FAT10 modification of its substrates and
promote the substrates be rapidly degraded. High expression of FAT10 can decrease the molecules positioning
on the kinetochore MAD2 and then increase chromosomal instability in the early and mid-term cell cycle. In
addition, FAT10 expression can lead to apoptosis and can be regulated by p53. Also, FAT10 could be upregulated
in liver cancer, gastric cancer and gynecological cancer. This review summarizes the advance of the ubiquitin-
like molecule (UBL) FAT10 in recent years.
Key words: FAT10；ubiquitin-like modifier；proteasome；apoptosis；cancer
蛋白质的翻译后修饰从一个新的角度揭示了蛋
白质的生物学调控机制。近年来，翻译后修饰与功
能变化的关系成为细胞生物学功能领域中的一大研
究热点。许多蛋白质生物功能的发挥是通过其自身
多肽基序的共价修饰，如泛素化、磷酸化、甲基
化和乙酰基化等。泛素化修饰是人们了解最多的修
饰类型之一。
泛素化修饰的典型代表是泛素蛋白介导的蛋白
质翻译后修饰。泛素是一个具有76个氨基酸残基的
多肽，广泛存在于真核生物中。在泛素具有的许多
功能中，了解最多的是靶蛋白经过泛素系统修饰进
而被蛋白酶体降解的过程。自从泛素在20 世纪70

Advance in the research of the ubiquitin-like molecule FAT10

泛素样分子FAT10研究进展

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