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纤连蛋白片段CH-296可抑制细胞凋亡,并增强鼠逆转录病毒和人慢病毒载体在非人类灵长类动物CD34+细胞中的离体基因转移,且与病毒嗜性无关。

Fibronectin fragment CH-296 inhibits apoptosis and enhances ex vivo gene transfer by murine retrovirus and human lentivirus vectors independent of viral tropism in nonhuman primate CD34+ cells.

作者信息

Donahue R E, Sorrentino B P, Hawley R G, An D S, Chen I S, Wersto R P

机构信息

Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 21892, USA.

出版信息

Mol Ther. 2001 Mar;3(3):359-67. doi: 10.1006/mthe.2001.0269.

Abstract

The fibronectin fragment CH-296 improved gene transfer to cytokine-mobilized nonhuman primate CD34+ cells irrespective of tropism to the MoMLV, GaLV, and VSV-G envelope proteins using murine stem cell virus (MSCV) and human immunodeficiency virus-1 (HIV-1)-based retrovirus vectors. For the HIV-1 lentivirus vector, CH-296 enhanced gene transfer in the absence of added hematopoietic growth factors necessary for ex vivo stem cell expansion. In the presence of CH-296, apoptosis of CD34+ cells was inhibited, and in mobilized peripheral blood CD34+ cells, cell division was stimulated as measured by cell history/tracking experiments.

摘要

纤连蛋白片段CH-296可改善细胞因子动员的非人灵长类动物CD34+细胞的基因转移,无论使用鼠干细胞病毒(MSCV)和基于人类免疫缺陷病毒-1(HIV-1)的逆转录病毒载体时对莫洛尼鼠白血病病毒(MoMLV)、猫白血病病毒(GaLV)和水疱性口炎病毒糖蛋白(VSV-G)包膜蛋白的嗜性如何。对于HIV-1慢病毒载体,CH-296在无体外干细胞扩增所需的造血生长因子添加的情况下增强了基因转移。在CH-296存在的情况下,CD34+细胞的凋亡受到抑制,并且在动员的外周血CD34+细胞中,通过细胞历史/追踪实验测量发现细胞分裂受到刺激。

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