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Title: Epstein–Barr virus nuclear antigen 3C interact with p73: Interplay between a viral oncoprotein and cellular tumor suppressor

Abstract

The p73 protein has structural and functional homology with the tumor suppressor p53, which plays an important role in cell cycle regulation, apoptosis, and DNA repair. The p73 locus encodes both a tumor suppressor (TAp73) and a putative oncogene (ΔNp73). p73 May play a significant role in p53-deficient lymphomas infected with Epstein–Barr virus (EBV). EBV produces an asymptomatic infection in the majority of the global population, but it is associated with several human B-cell malignancies. The EBV-encoded Epstein–Barr virus nuclear antigen 3C (EBNA3C) is thought to disrupt the cell cycle checkpoint by interacting directly with p53 family proteins. Doxorubicin, a commonly used chemotherapeutic agent, induces apoptosis through p53 and p73 signaling such that the lowΔNp73 level promotes the p73-mediated intrinsic pathway of apoptosis. In this report, we investigated the mechanism by which EBV infection counters p73α-induced apoptosis through EBNA3C. - Highlights: • EBV-encoded EBNA3C suppresses doxorubicin-induced apoptosis in B-cell lymphomas. • EBNA3C binds to p73 to suppress its apoptotic effect. • EBNA3C maintains latency by regulating downstream mitochondrial pathways.

Authors:
; ;  [1];  [2];  [3];  [1]
  1. Division of Infectious Disease Biology, Institute of Life Sciences, Nalco Square, Chandrasekharpur, Bhubaneswar 751023 (India)
  2. School of Biotechnology, KIIT University, Bhubaneswar (India)
  3. Department of Microbiology and Immunology, University of Nevada, School of Medicine, Reno, NV 89557 (United States)
Publication Date:
OSTI Identifier:
22435004
Resource Type:
Journal Article
Journal Name:
Virology
Additional Journal Information:
Journal Volume: 448; Other Information: Copyright (c) 2013 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0042-6822
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANTIGENS; APOPTOSIS; CELL CYCLE; DNA REPAIR; DOXORUBICIN; LYMPHOMAS; MITOCHONDRIA; ONCOGENES; PROTEINS; SIGNALS; VIRUSES

Citation Formats

Sahu, Sushil Kumar, Mohanty, Suchitra, Kumar, Amit, Kundu, Chanakya N., Verma, Subhash C., Choudhuri, Tathagata, and Department of Biotechnology, Siksha Bhavana, Visva Bharati, Santiniketan, Bolpur. Epstein–Barr virus nuclear antigen 3C interact with p73: Interplay between a viral oncoprotein and cellular tumor suppressor. United States: N. p., 2014. Web. doi:10.1016/J.VIROL.2013.10.023.
Sahu, Sushil Kumar, Mohanty, Suchitra, Kumar, Amit, Kundu, Chanakya N., Verma, Subhash C., Choudhuri, Tathagata, & Department of Biotechnology, Siksha Bhavana, Visva Bharati, Santiniketan, Bolpur. Epstein–Barr virus nuclear antigen 3C interact with p73: Interplay between a viral oncoprotein and cellular tumor suppressor. United States. https://doi.org/10.1016/J.VIROL.2013.10.023
Sahu, Sushil Kumar, Mohanty, Suchitra, Kumar, Amit, Kundu, Chanakya N., Verma, Subhash C., Choudhuri, Tathagata, and Department of Biotechnology, Siksha Bhavana, Visva Bharati, Santiniketan, Bolpur. 2014. "Epstein–Barr virus nuclear antigen 3C interact with p73: Interplay between a viral oncoprotein and cellular tumor suppressor". United States. https://doi.org/10.1016/J.VIROL.2013.10.023.
@article{osti_22435004,
title = {Epstein–Barr virus nuclear antigen 3C interact with p73: Interplay between a viral oncoprotein and cellular tumor suppressor},
author = {Sahu, Sushil Kumar and Mohanty, Suchitra and Kumar, Amit and Kundu, Chanakya N. and Verma, Subhash C. and Choudhuri, Tathagata and Department of Biotechnology, Siksha Bhavana, Visva Bharati, Santiniketan, Bolpur},
abstractNote = {The p73 protein has structural and functional homology with the tumor suppressor p53, which plays an important role in cell cycle regulation, apoptosis, and DNA repair. The p73 locus encodes both a tumor suppressor (TAp73) and a putative oncogene (ΔNp73). p73 May play a significant role in p53-deficient lymphomas infected with Epstein–Barr virus (EBV). EBV produces an asymptomatic infection in the majority of the global population, but it is associated with several human B-cell malignancies. The EBV-encoded Epstein–Barr virus nuclear antigen 3C (EBNA3C) is thought to disrupt the cell cycle checkpoint by interacting directly with p53 family proteins. Doxorubicin, a commonly used chemotherapeutic agent, induces apoptosis through p53 and p73 signaling such that the lowΔNp73 level promotes the p73-mediated intrinsic pathway of apoptosis. In this report, we investigated the mechanism by which EBV infection counters p73α-induced apoptosis through EBNA3C. - Highlights: • EBV-encoded EBNA3C suppresses doxorubicin-induced apoptosis in B-cell lymphomas. • EBNA3C binds to p73 to suppress its apoptotic effect. • EBNA3C maintains latency by regulating downstream mitochondrial pathways.},
doi = {10.1016/J.VIROL.2013.10.023},
url = {https://www.osti.gov/biblio/22435004}, journal = {Virology},
issn = {0042-6822},
number = ,
volume = 448,
place = {United States},
year = {Sun Jan 05 00:00:00 EST 2014},
month = {Sun Jan 05 00:00:00 EST 2014}
}