Turnover of Hepatitis B Virus X Protein Is Regulated by Damaged DNA-Binding Complex

DDB1 HBx Woodchuck hepatitis virus
DOI: 10.1128/jvi.76.13.6495-6501.2002 Publication Date: 2002-07-27T10:09:29Z
ABSTRACT
ABSTRACT Mammalian hepatitis B viruses encode an essential regulatory protein, termed X, which may also be implicated in liver cancer development associated with chronic infection. X referred to as HBx human virus and WHx woodchuck virus, has been reported bind a number of cellular proteins, including the DDB1 subunit damaged DNA-binding (DDB) complex. Our previous work provided genetic evidence for importance WHx-DDB1 interaction both activity protein establishment viral infection woodchucks. In present study, direct action on is documented. Physical between two proteins leads increase stability. This effect results from protection proteasome-mediated degradation. Protection overcome presence DDB2, second DDB heterodimer. keeping observations HBx, DDB2 was found directly WHx. Nonetheless, counteracting stabilization requires DDB2-DDB1 interaction. Taken together, these findings substantiate physical functional connection DDB1-DDB2 heterodimer, leading regulation pool protein.
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