Other Publications (1)
Articles by Hsin-Tien Chen in JoVE
In situ subcellulaire fractionering van het aanklevende en niet-klevende zoogdiercellen 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 In situ subcellulaire fractionatie van zoogdiercellen op microscoop dekglaasjes kan de visualisatie van eiwit lokalisatie.
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.