Gene expression profile of HIV-1 Tat expressing cells: a close interplay between proliferative and differentiation signals

被引:44
作者
de la Fuente, Cynthia [2 ]
Santiago, Francisco [2 ]
Deng, Longwen [2 ]
Eadie, Carolyne [2 ]
Zilberman, Irene [2 ]
Kehn, Kylene [2 ]
Maddukuri, Anil [2 ]
Baylor, Shanese [2 ]
Wu, Kaili [2 ]
Lee, Chee Gun [1 ]
Pumfery, Anne [2 ]
Kashanchi, Fatah [2 ]
机构
[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Biochem & Mol Biol, Newark, NJ 07103 USA
[2] George Washington Univ, Sch Med, Dept Biochem & Mol Biol, Washington, DC 20037 USA
来源
BMC BIOCHEMISTRY | 2002年 / 3卷
关键词
D O I
10.1186/1471-2091-3-14
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Expression profiling holds great promise for rapid host genome functional analysis. It is plausible that host expression profiling in an infection could serve as a universal phenotype in virally infected cells. Here, we describe the effect of one of the most critical viral activators, Tat, in HIV-1 infected and Tat expressing cells. We utilized microarray analysis from uninfected, latently HIV-1 infected cells, as well as cells that express Tat, to decipher some of the cellular changes associated with this viral activator. Results: Utilizing uninfected, HIV-1 latently infected cells, and Tat expressing cells, we observed that most of the cellular host genes in Tat expressing cells were down-regulated. The down-regulation in Tat expressing cells is most apparent on cellular receptors that have intrinsic receptor tyrosine kinase (RTK) activity and signal transduction members that mediate RTK function, including Ras-Raf-MEK pathway. Co-activators of transcription, such as p300/CBP and SRC-1, which mediate gene expression related to hormone receptor genes, were also found to be down-regulated. Down-regulation of receptors may allow latent HIV-1 infected cells to either hide from the immune system or avoid extracellular differentiation signals. Some of the genes that were up-regulated included co-receptors for HIV-1 entry, translation machinery, and cell cycle regulatory proteins. Conclusions: We have demonstrated, through a microarray approach, that HIV-1 Tat is able to regulate many cellular genes that are involved in cell signaling, translation and ultimately control the host proliferative and differentiation signals.
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页码:1 / 22
页数:22
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