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EDAG促进人CD34+细胞的扩增和存活。

EDAG promotes the expansion and survival of human CD34+ cells.

作者信息

Zhao Ke, Zheng Wei-Wei, Dong Xiao-Ming, Yin Rong-Hua, Gao Rui, Li Xiu, Liu Jin-Fang, Zhan Yi-Qun, Yu Miao, Chen Hui, Ge Chang-Hui, Ning Hong-Mei, Yang Xiao-Ming, Li Chang-Yan

机构信息

State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.

Tianjin University, School of Chemical Engineering and Technology, Department of Pharmaceutical Engineering, Tianjin, China.

出版信息

PLoS One. 2018 Jan 11;13(1):e0190794. doi: 10.1371/journal.pone.0190794. eCollection 2018.

Abstract

EDAG is multifunctional transcriptional regulator primarily expressed in the linloc-kit+Sca-1+ hematopoietic stem cells (HSC) and CD34+ progenitor cells. Previous studies indicate that EDAG is required for maintaining hematopoietic lineage commitment balance. Here using ex vivo culture and HSC transplantation models, we report that EDAG enhances the proliferative potential of human cord blood CD34+ cells, increases survival, prevents cell apoptosis and promotes their repopulating capacity. Moreover, EDAG overexpression induces rapid entry of CD34+ cells into the cell cycle. Gene expression profile analysis indicate that EDAG knockdown leads to down-regulation of various positive cell cycle regulators including cyclin A, B, D, and E. Together these data provides novel insights into EDAG in regulation of expansion and survival of human hematopoietic stem/progenitor cells.

摘要

EDAG是一种多功能转录调节因子,主要表达于linloc-kit+Sca-1+造血干细胞(HSC)和CD34+祖细胞中。先前的研究表明,EDAG是维持造血谱系定向平衡所必需的。在此,我们利用体外培养和HSC移植模型报告称,EDAG增强了人脐血CD34+细胞的增殖潜力,提高了存活率,防止细胞凋亡并促进了它们的再增殖能力。此外,EDAG的过表达诱导CD34+细胞快速进入细胞周期。基因表达谱分析表明,EDAG的敲低导致包括细胞周期蛋白A、B、D和E在内的各种阳性细胞周期调节因子的下调。这些数据共同为EDAG在调节人类造血干/祖细胞的扩增和存活方面提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbdc/5764277/b8b98b9dacef/pone.0190794.g001.jpg

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