Cyclin B1, an important cell cycle regulator, was up-regulated in lymphocytes of human immunodeficiency virus (HIV)-infected patients. However, the mechanism of cyclin B1 up-regulation and the effects of the up-regulation on the host cells remain unclear. Here, we show that HIV-encoded Tat protein regulates cyclin B1 levels in two different ways: first, Tat stimulates the transcription of cyclin B1, which increases cyclin B1 levels and promotes the cells apoptosis; and second, Tat stimulates polyubiquitination-mediated degradation of cyclin B1 through binding to the N-terminal of cyclin B1 (aa 61–129) that is just downstream of the D box, which prevents excessive levels of cyclin B1 in the cells. These results suggest that Tat-regulating cyclin B1 affects the status of HIV: Tat stimulates cyclin B1 expression to slow down the host cell cycle progress and to promote the host cell apoptosis, which might facilitate HIV release; Tat stimulates cyclin B1 degradation to prevent overaccumulation of cyclin B1, which might facilitate HIV replication. Taken together, our results reveal for the first time how HIV-Tat regulates cyclin B1 and keeps its balance in the cells.—Zhang, S.-M., Sun, Y., Fan, R., Xu, Q.-Z., Liu, X.-D., Zhang, X., Wang, Y., Zhou, P.-K. HIV-1 Tat regulates cyclin B1 by promoting both expression and degradation.
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HIV-1 Tat regulates cyclin B1 by promoting both expression and degradation
Zhang, Shi-Meng; Sun, Yi; Fan, Rong; Xu, Qin-Zhi; Liu, Xiao-Dan; Zhang, Xiangming; Wang, Ya; Zhou, Ping-Kun
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, Volume 24 (2): 495
Fed of American Socs for Experimental Biology – Feb 1, 2010
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