hCLP46 increases Smad3 protein stability via inhibiting its ubiquitin-proteasomal degradation

作     者：Yingying Xing Qiaoyun Chu Run Feng Wei Wang Lixin Liu Zhongbing Lu 

作者机构：College of Life Sciences University of Chinese Academy of Science Beijing 100049 China Key Laboratory for Polymeric Composite and Functional Materialsof Ministry of Education School of Chemistry and ChemicalEngineering Sun Yat-Sen University Guangzhou 510275 China School of Medical Science Edith Cowan University Joondalup WA 6027 Australia Department of Biochemistry and Molecular Biology Capital Medical University Beijing 10069 China 

出 版 物：《Protein & Cell》 (蛋白质与细胞（英文版）)

年 卷 期：2015年第6卷第10期

页      面：767-770页

核心收录：

学科分类：0710[理学-生物学] 07[理学] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种] 071002[理学-动物学] 

基　　金：This study was supported by grants from National Natural Science Foundation of China (Grant Nos.30670889  81270319 and 81470520)  Guangdong Innovation Team Project (2013S086) Guandong Natural Science Foundation (2014A030312018)  the National 'Twelfth Five-Year' Plan for Science and Technology Support (2012BAI37B03) and the Hundred Talents Program of Chinese Academy of Sciences 

主　　题：Acute Myeloid Leukemia Notch Signaling DAPT Smad3 Protein Smad3 Expression 

摘      要：hCLP46 （human CAP10-1ike protein 46 kDa） was initially isolated and identified from human acute myeloid leukemia transformed from myelodysplastic syndrome （MDS-AML） CD34＋ cells （Teng et al., 2006） and we demonstrated previ- ously that hCLP46 is abnormally expressed in many hematopoietic malignancies （Wang et al., 2010）.