Other Publications (1)
Articles by Hsin-Tien Chen in JoVE
Yapışkan ve Sigara yapışık Memeli Hücre yerinde Subselüler Fraksiyonu Anyaporn Sawasdichai1, Hsin-Tien Chen1, Nazefah Abdul Hamid1, Padma-Sheela Jayaraman2, Kevin Gaston1 1Department of Biochemistry, School of Medical Sciences, University of Bristol, 2Division of Immunity and Infection, School of Medicine, University of Birmingham , Memeli hücrelerinin mikroskop lamelleri yerinde Subselüler fraksiyonasyon protein localisation görselleştirme sağlar .
Other articles by Hsin-Tien Chen on PubMed
E2 Proteins from High- and Low-risk Human Papillomavirus Types Differ in Their Ability to Bind P53 and Induce Apoptotic Cell Death Journal of Virology. May, 2006 | Pubmed ID: 16611918 The E2 proteins from oncogenic (high-risk) human papillomaviruses (HPVs) can induce apoptotic cell death in both HPV-transformed and non-HPV-transformed cells. Here we show that the E2 proteins from HPV type 6 (HPV6) and HPV11, two nononcogenic (low-risk) HPV types, fail to induce apoptosis. Unlike the high-risk HPV16 E2 protein, these low-risk E2 proteins fail to bind p53 and fail to induce p53-dependent transcription activation. Interestingly, neither the ability of p53 to activate transcription nor the ability of p53 to bind DNA, are required for HPV16 E2-induced apoptosis in non-HPV-transformed cells. However, mutations that reduce the binding of the HPV16 E2 protein to p53 inhibit E2-induced apoptosis in non-HPV-transformed cells. In contrast, the interaction between HPV16 E2 and p53 is not required for this E2 protein to induce apoptosis in HPV-transformed cells. Thus, our data suggest that this high-risk HPV E2 protein induces apoptosis via two pathways. One pathway involves the binding of E2 to p53 and can operate in both HPV-transformed and non-HPV-transformed cells. The second pathway requires the binding of E2 to the viral genome and can only operate in HPV-transformed cells.