Functional cross-talk between p73 beta and NF-kappa B mediated by p300
- Authors
- Ryou, Sang-Mi; Kang, Kyung-Hwa; Jeong, Mi-Hee; Kim, Jung Woong; An, Joo-Hee; Lee, So-Youn; Jang, Sangmin; Song, Peter I.; Choi, Kyung-Hee
- Issue Date
- Jun-2006
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- p73; NF-kappa B RelA(p65); p300
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.345, no.2, pp 623 - 630
- Pages
- 8
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 345
- Number
- 2
- Start Page
- 623
- End Page
- 630
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/52732
- DOI
- 10.1016/j.bbrc.2006.04.120
- ISSN
- 0006-291X
1090-2104
- Abstract
- p73 beta is associated with induction of apoptosis or cellular growth arrest, while NF-kappa B is closely related with promotion of resistance to programmed cell death. These biologically opposing activities between p73 beta and NF-kappa B propose a regulatory mechanism of critical turning on/off in cellular apoptotic or survival responses. In this study, we demonstrate that NF-kappa B-mediated transactivation is specifically downreaulated by p73 beta; conversely, p73 beta-transactivation is negatively regulated by functional expression of p65, NF-kappa B RelA subunit. The p73 beta transactivation domain (TA) and p65 NH-terminus are crucial for their negative regulation of p65- and p73 beta-mediated transactivation, respectively. Furthermore, p65- or p73 beta-interaction with p300 is reciprocally inhibited by their competitive binding to p300 in a restrict amount-dependent manner. Likewise, both p73 beta-activated apoptosis and p65-dependent increase of cell viability Lire reciprocally repressed by p65 and p73 beta, respectively. These results have important implications for p300-mediated regulatory mechanism between p73 beta- and p65-transactivation, by which both p73 beta and NF-kappa B could Mutually affect on their biological activities. Therefore, we propose that p300 is a transactivational regulator of competitively balanced cross-talk between p73 beta and p65.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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