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Borna Disease Virus Phosphoprotein Represses p53-Mediated Transcriptional Activity by Interference with HMGB1

Guoqi Zhang, Takeshi Kobayashi, Wataru Kamitani, Satoshi Komoto, Makiko Yamashita, Satoko Baba, Hideyuki Yanai, Kazuyoshi Ikuta, and Keizo Tomonaga

Journal of Virology, November 2003, p. 12243-12251, Vol. 77, No. 22


In this study, researchers used plasmid recombinant technology to generate HMGB1, p53, and P. HMGB1 is a growth factor, p53 is a tumor suppression factor that is enhanced through binding with HMGB1, and P is a 24-kDA phosphoprotein found in bornaviruses that inhibits HMGB1. The study aimed to determine the mechanism by which P inhibits HMGB1, with the hypothesis that P interferes with the binding between p53 and HMGB1.
The hypothesis was confirmed using a variety of techniques and assays, including recombinant plasmid technology to generate proteins, p53 deficient cells, and a Far Western blot. p53 and P was found to competitively bind with HMGB on the A box domain. P also decreased p53-mediated activation of cyclin G promoters, and p53 failed to upregulate cell-cycle inhibitor p21wafl in infected cells.

Development of this mechanism provides an understanding of not only the roles of HMGB1, but also that of P in vitro and how their interactions through p53 result in the virus’s neuropathogenicity. The study also established P as unique for its competitive binding with p53, for most viruses interfere with p53 by binding directly; a common mechanism found in oncogenic viruses.

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