We previously found that HPV16 E6 causes the degradation of the tumor suppressor protein TSC2,resulting in the phosphorylation of S6 kinase and S6 even in the absence of insulin.In the present study,we investigated th...We previously found that HPV16 E6 causes the degradation of the tumor suppressor protein TSC2,resulting in the phosphorylation of S6 kinase and S6 even in the absence of insulin.In the present study,we investigated the role of E6AP in HPV16 E6 induced TSC2 degradation.Our results demonstrated that TSC2 was targeted for degradation in the presence or absence of HPV16 E6.Over-expression of E6AP enhanced the degradation of TSC2 by HPV16 E6,while expression of a dominant negative E6AP(C833A)inhibited the E6-induced degradation.Additionally,by using shRNAs to block E6AP expression in HPV16 positive and negative cells,we found a significantly prolonged TSC2 half life.展开更多
文摘We previously found that HPV16 E6 causes the degradation of the tumor suppressor protein TSC2,resulting in the phosphorylation of S6 kinase and S6 even in the absence of insulin.In the present study,we investigated the role of E6AP in HPV16 E6 induced TSC2 degradation.Our results demonstrated that TSC2 was targeted for degradation in the presence or absence of HPV16 E6.Over-expression of E6AP enhanced the degradation of TSC2 by HPV16 E6,while expression of a dominant negative E6AP(C833A)inhibited the E6-induced degradation.Additionally,by using shRNAs to block E6AP expression in HPV16 positive and negative cells,we found a significantly prolonged TSC2 half life.
