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Enhanced production of p24 Gag protein in HIV-1-infected rat cells fused with uninfected human cells.
Title: | Enhanced production of p24 Gag protein in HIV-1-infected rat cells fused with uninfected human cells. |
Authors: | Chen, Jing Browse this author | Zhao, Xudong Browse this author | Lai, Yurong Browse this author | Suzuki, Akira Browse this author | Tomaru, Utano Browse this author | Ishizu, Akihiro Browse this author →KAKEN DB | Takada, Akio Browse this author | Ikeda, Hitoshi Browse this author | Kasahara, Masanori Browse this author | Yoshiki, Takashi Browse this author |
Keywords: | HIV-1 | Rat model | Cell fusion | Cyclin T1 | CDK9 | CRM1 | HP68 | CIITA |
Issue Date: | Aug-2007 |
Publisher: | Elsevier Inc. |
Journal Title: | Experimental and Molecular Pathology |
Volume: | 83 |
Issue: | 1 |
Start Page: | 125 |
End Page: | 130 |
Publisher DOI: | 10.1016/j.yexmp.2006.11.003 |
PMID: | 17222823 |
Abstract: | Although many human molecules have been suggested to affect replication of human immunodeficiency virus type 1 (HIV-1), the distribution of such cofactors in human cell types is not well understood. Rat W31/D4R4 fibroblasts expressing human CD4 and CXCR4 receptors were infected with HIV-1. The provirus was integrated in the host genome, but only a limited amount of p24 Gag protein was produced in the cells and culture supernatants. Here we found that p24 production was significantly increased by fusing HIV-1-infected W31/D4R4 cells with uninfected human cell lines of T-cell, B-cell, or macrophage lineages. These findings suggest that human cellular factors supporting HIV-1 replication are distributed widely in cells of lymphocyte and macrophage lineages. We also examined whether the amount of p24 produced by rat–human hybrid cells was correlated with expression levels of specific human genes. The results suggested that HP68 and MHC class II transactivator (CIITA) might up- and down-regulate p24 production, respectively. It was also suggested that HIV-1 replication is affected by molecules other than those examined in this study, namely, cyclin T1, cyclin-dependent kinase 9, CRM1, HP68, and CIITA. |
Relation: | http://www.sciencedirect.com/science/journal/00144800 |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/28263 |
Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 石津 明洋
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