NRIP enhances HPV gene expression via interaction with either GR or E2
Journal
Virology
Journal Volume
423
Journal Issue
1
Pages
38-48
Date Issued
2012
Author(s)
Abstract
We previously identified a gene, nuclear receptor-interaction protein (NRIP), which functions as a transcription cofactor in glucocorticoid receptor (GR) and human papillomavirus E2 (HPV E2)-driven gene expression. Here, we comprehensively evaluated the role of NRIP in HPV-16 gene expression. NRIP acts as a transcription cofactor to enhance GR-regulated HPV-16 gene expression in the presence of hormone. NRIP also can form complex with E2 that caused NRIP-induced HPV gene expression via E2-binding sites in a hormone-independent manner. Furthermore, NRIP can associate with GR and E2 to form tri-protein complex to activate HPV gene expression via GRE, not the E2-binding site, in a hormone-dependent manner. These results indicate that NRIP and GR are viral E2-binding proteins and that NRIP regulates HPV gene expression via GRE and/or E2 binding site in the HPV promoter in a hormone-dependent or independent manner, respectively. ? 2011 Elsevier Inc.
Subjects
E2; GR; Hormone; HPV-16; NRIP
SDGs
Other Subjects
dexamethasone; glucocorticoid receptor; protein E2; receptor interacting protein; transcription factor; unclassified drug; virus protein; article; binding site; cancer cell culture; cell proliferation; chromatin immunoprecipitation; complex formation; controlled study; gene expression; gene expression regulation; human; human cell; Human papillomavirus type 16; nucleotide sequence; priority journal; promoter region; protein function; protein protein interaction; receptor binding; reverse transcription polymerase chain reaction; virus genome; Wart virus; Western blotting; Adaptor Proteins, Signal Transducing; Cell Line; DNA-Binding Proteins; Gene Expression Regulation, Viral; Human papillomavirus 16; Humans; Molecular Sequence Data; Nuclear Proteins; Oncogene Proteins, Viral; Papillomavirus Infections; Protein Binding; Receptors, Glucocorticoid; Transcription, Genetic; Up-Regulation; Human papillomavirus; Human papillomavirus type 16
Type
journal article