TAp63alpha Induced Apoptosis Inhibited by Kaposi's Sarcoma Herpesvirus Latency Nuclear AntigenSuchitra Mohanty1#, Sushil Kumar Sahu1#, Nabanita Roy Chattopadhyay2#, Amit Kumar1, Piyanki Das2 and Tathagata Choudhuri1,2*
- *Corresponding Author:
- Tathagata Choudhuri
Department of Biotechnology, Siksha Vhabana
Visva Bharati, Santiniketan, Bolpur, India
E-mail: [email protected]
Received date: March 02, 2015; Accepted date: March 27, 2015; Published date: April 02, 2015
Citation: Mohanty S, Sahu SK, Chattopadhyay NR, Kumar A, Choudhuri T, et al. (2015) TAp63alpha Induced Apoptosis Inhibited by Kaposi’s Sarcoma Herpesvirus Latency Nuclear Antigen. J Carcinog Mutagen 6:221. doi: 10.4172/2157-2518.1000221
Copyright: © 2015 Choudhuri T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Kaposi’s sarcoma-associated herpesvirus (KSHV) infects a variety of human cells including cells of epithelial, mesenchymal and endothelial origin. The latency associated nuclear antigen (LANA) of this virus regulates the transcription of a number of viral and cellular genes essential for the survival of the virus in the host cell. TAp63α can induce apoptosis in stressed cells by upregulating various death receptors and loss of mitochondrial membrane potential. The present study demonstrates that LANA inhibits TAp63α-mediated apoptosis by a direct interaction with each other. This interaction also results in a reduction in loss of mitochondrial membrane potential caused by TAp63α. Therefore the present study indicates a possible mechanism of KSHV-infected cells to escape apoptosis and facilitate survival.