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Related Experiment Video

Updated: May 26, 2026

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions

Published on: July 18, 2013

NRIP enhances HPV gene expression via interaction with either GR or E2.

Szu-Wei Chang¹, Pei-Yu Lu, Jih-Huong Guo

¹Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.

|December 20, 2011

Summary

Nuclear receptor-interaction protein (NRIP) enhances human papillomavirus (HPV) gene expression. NRIP acts with glucocorticoid receptor (GR) or HPV E2 protein, regulating viral gene activity.

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Area of Science:

Molecular Biology
Virology
Gene Regulation

Background:

Nuclear receptor-interaction protein (NRIP) is a known transcription cofactor.
NRIP participates in glucocorticoid receptor (GR) and human papillomavirus E2 (HPV E2) mediated gene expression.

Purpose of the Study:

To comprehensively evaluate the role of NRIP in HPV-16 gene expression.
To elucidate the mechanisms by which NRIP influences HPV-16 transcription.

Main Methods:

Assessed NRIP's function as a transcription cofactor.
Investigated NRIP's interaction with GR and HPV E2 protein.
Analyzed NRIP's effect on HPV-16 gene expression in hormone-dependent and independent manners.

Main Results:

NRIP enhances GR-regulated HPV-16 gene expression in a hormone-dependent manner.
NRIP induces HPV gene expression via E2-binding sites independently of hormones.
NRIP forms a tri-protein complex with GR and E2 to activate HPV gene expression via GRE in a hormone-dependent manner.

Conclusions:

NRIP and GR are identified as viral E2-binding proteins.
NRIP regulates HPV gene expression through GRE and/or E2 binding sites in the HPV promoter.
Regulation is dependent on hormone presence or absence.