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. 2006 Nov 10;366(1):67–81. doi: 10.1016/j.jmb.2006.11.011

Figure 9.

Figure 9

Model for the cytoprotective mechanism exerted by HIV-1 infection and intracellular HIV-1 Tat expression in microglial cells. HIV-1 infection or expression of intracellular HIV-1 Tat results in decreased PTEN expression which alleviates the restraint on activation of the PI-3-K/Akt pathway. The increased activation of PI-3-K and Akt leads to long-term cellular survival.85 Intracellular Tat can also decrease activity of p53, which in turn leads to progression through the cell cycle, activating the E2F transcription factor and proliferation-specific signals.86 E2F also regulates survival by transcriptionally activating an upstream adaptor protein involved in the activation of the PI-3-K/Akt pathway.52 The combined modulation of PTEN and p53 by expression of Tat leads to the increased activation of proliferation and long-term cellular survival exhibited in microglia during HIV-1 infection: dotted lines, negative regulation; thick arrows, positive regulation; thin arrows, effects of intracellular Tat expression and HIV-1 infection.