中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2010, 22(2): 124-128
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-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
 
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-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
 
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