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Fig. 6 | Molecular Medicine

Fig. 6

From: Heat-shock protein 90α is involved in maintaining the stability of VP16 and VP16-mediated transactivation of α genes from herpes simplex virus-1

Fig. 6

Hsp90 inhibition ameliorated HSV-1 infection-induced skin lesions in mice. a, b Hsp90 inhibitors failed to reduce α gene expression and led to VP16 degradation in autophagy-deficient cells. a MEF WT and ATG7−/− cells were infected with HSV-1 (MOI 50) for 2 h in the presence or absence of AT533 (2 μM) or not and then total RNA was extracted and analyze by qRT-PCR to determine the level of α gene expression, including α0 and α4. b MEF WT and ATG7−/− cells were infected with HSV-1 (MOI 50) for 2 h in the presence of AT533 (2 μM), and total protein was extracted for western blot analysis to detect the level of VP16. c HSV-1-infected mice were treated with gels containing the indicated concentrations of AT533 on the infected skin once per day. Mice were sacrificed on day 7 after HSV-1 infection and then the zosteriform lesions were evaluated and snapped (c). The size of the zosteriform lesions was quantified by determining the widths of the zosteriform lesions from three mice and are expressed as means ± SD (D). e Approximately a 1 cm square piece of skin tissue was obtained as described in section 2.9 of the Materials and Methods, and total RNA was extracted. The relative expression of the α0, α4 and VP16 genes was determined by real-time PCR (n = 3 mice). f Approximately a 1 cm square piece of skin tissue was obtained and then analyzed for viral titers with the method described in section 2.5 of the Materials and Methods (n = 3 mice). g The corresponding skin samples were obtained from mice as described in section 2.9 of the Materials and Methods then the total protein was extracted to analyze the level of VP16 using western blotting (n = 4 mice)

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