A functional interferon regulatory factor-1 (IRF-1)-binding site in the upstream regulatory region (URR) of human papillomavirus type 16

Istvan Arany, Kenneth J. Grattendick, William E. Whitehead, I. Ember, Stephen K. Tyring

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

We recently identified a new enhancer element (HIRE-1, HPV-Interferon Responsive Element-1) in the upstream regulatory region (URR) of human papillomavirus (HPV) type 16. HIRE-1 is located upstream from and in close proximity to the TATA box. HIRE-1 is 1 nt shorter in its 5′ sequence in comparison to a consensus IRF-1 binding site (IRF-E). Gel shift analyses clearly demonstrated that HIRE-1 is capable of binding IRF-1 in response to interferon-γ (IFN-γ) treatment. In a reporter system, HIRE-1 stimulated transcription in response to IRF-1 or IFNγ from both a heterologous or the homologous (p97) promoter in a dose-dependent manner. Mutations in the core binding sequence strongly decreased this enhancer activity. Interestingly, HIRE-1 stimulated transcription in the context of the full URR in a cell-type-specific manner, thereby suggesting the role of other cell-type-specific factors that might counteract with its function. Thus, our results may explain the inconsistent clinical and experimental results observed following IFN treatment of cervical lesions or cells. Also, this new enhancer may have an important function during inflammatory responses against HPV type 16.

Original languageEnglish
Pages (from-to)280-286
Number of pages7
JournalVirology
Volume310
Issue number2
DOIs
Publication statusPublished - Jun 5 2003

Fingerprint

Interferon Regulatory Factor-1
Human papillomavirus 16
Nucleic Acid Regulatory Sequences
Interferons
Binding Sites
TATA Box
Electrophoretic Mobility Shift Assay
Mutation

Keywords

  • Enhancer
  • HPV16
  • Interferon
  • IRF-1
  • IRF-E
  • Promoter
  • Transcription

ASJC Scopus subject areas

  • Virology

Cite this

A functional interferon regulatory factor-1 (IRF-1)-binding site in the upstream regulatory region (URR) of human papillomavirus type 16. / Arany, Istvan; Grattendick, Kenneth J.; Whitehead, William E.; Ember, I.; Tyring, Stephen K.

In: Virology, Vol. 310, No. 2, 05.06.2003, p. 280-286.

Research output: Contribution to journalArticle

Arany, Istvan ; Grattendick, Kenneth J. ; Whitehead, William E. ; Ember, I. ; Tyring, Stephen K. / A functional interferon regulatory factor-1 (IRF-1)-binding site in the upstream regulatory region (URR) of human papillomavirus type 16. In: Virology. 2003 ; Vol. 310, No. 2. pp. 280-286.
@article{7fa5661a18f640169339c321176033ca,
title = "A functional interferon regulatory factor-1 (IRF-1)-binding site in the upstream regulatory region (URR) of human papillomavirus type 16",
abstract = "We recently identified a new enhancer element (HIRE-1, HPV-Interferon Responsive Element-1) in the upstream regulatory region (URR) of human papillomavirus (HPV) type 16. HIRE-1 is located upstream from and in close proximity to the TATA box. HIRE-1 is 1 nt shorter in its 5′ sequence in comparison to a consensus IRF-1 binding site (IRF-E). Gel shift analyses clearly demonstrated that HIRE-1 is capable of binding IRF-1 in response to interferon-γ (IFN-γ) treatment. In a reporter system, HIRE-1 stimulated transcription in response to IRF-1 or IFNγ from both a heterologous or the homologous (p97) promoter in a dose-dependent manner. Mutations in the core binding sequence strongly decreased this enhancer activity. Interestingly, HIRE-1 stimulated transcription in the context of the full URR in a cell-type-specific manner, thereby suggesting the role of other cell-type-specific factors that might counteract with its function. Thus, our results may explain the inconsistent clinical and experimental results observed following IFN treatment of cervical lesions or cells. Also, this new enhancer may have an important function during inflammatory responses against HPV type 16.",
keywords = "Enhancer, HPV16, Interferon, IRF-1, IRF-E, Promoter, Transcription",
author = "Istvan Arany and Grattendick, {Kenneth J.} and Whitehead, {William E.} and I. Ember and Tyring, {Stephen K.}",
year = "2003",
month = "6",
day = "5",
doi = "10.1016/S0042-6822(03)00138-7",
language = "English",
volume = "310",
pages = "280--286",
journal = "Virology",
issn = "0042-6822",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - A functional interferon regulatory factor-1 (IRF-1)-binding site in the upstream regulatory region (URR) of human papillomavirus type 16

AU - Arany, Istvan

AU - Grattendick, Kenneth J.

AU - Whitehead, William E.

AU - Ember, I.

AU - Tyring, Stephen K.

PY - 2003/6/5

Y1 - 2003/6/5

N2 - We recently identified a new enhancer element (HIRE-1, HPV-Interferon Responsive Element-1) in the upstream regulatory region (URR) of human papillomavirus (HPV) type 16. HIRE-1 is located upstream from and in close proximity to the TATA box. HIRE-1 is 1 nt shorter in its 5′ sequence in comparison to a consensus IRF-1 binding site (IRF-E). Gel shift analyses clearly demonstrated that HIRE-1 is capable of binding IRF-1 in response to interferon-γ (IFN-γ) treatment. In a reporter system, HIRE-1 stimulated transcription in response to IRF-1 or IFNγ from both a heterologous or the homologous (p97) promoter in a dose-dependent manner. Mutations in the core binding sequence strongly decreased this enhancer activity. Interestingly, HIRE-1 stimulated transcription in the context of the full URR in a cell-type-specific manner, thereby suggesting the role of other cell-type-specific factors that might counteract with its function. Thus, our results may explain the inconsistent clinical and experimental results observed following IFN treatment of cervical lesions or cells. Also, this new enhancer may have an important function during inflammatory responses against HPV type 16.

AB - We recently identified a new enhancer element (HIRE-1, HPV-Interferon Responsive Element-1) in the upstream regulatory region (URR) of human papillomavirus (HPV) type 16. HIRE-1 is located upstream from and in close proximity to the TATA box. HIRE-1 is 1 nt shorter in its 5′ sequence in comparison to a consensus IRF-1 binding site (IRF-E). Gel shift analyses clearly demonstrated that HIRE-1 is capable of binding IRF-1 in response to interferon-γ (IFN-γ) treatment. In a reporter system, HIRE-1 stimulated transcription in response to IRF-1 or IFNγ from both a heterologous or the homologous (p97) promoter in a dose-dependent manner. Mutations in the core binding sequence strongly decreased this enhancer activity. Interestingly, HIRE-1 stimulated transcription in the context of the full URR in a cell-type-specific manner, thereby suggesting the role of other cell-type-specific factors that might counteract with its function. Thus, our results may explain the inconsistent clinical and experimental results observed following IFN treatment of cervical lesions or cells. Also, this new enhancer may have an important function during inflammatory responses against HPV type 16.

KW - Enhancer

KW - HPV16

KW - Interferon

KW - IRF-1

KW - IRF-E

KW - Promoter

KW - Transcription

UR - http://www.scopus.com/inward/record.url?scp=85047689512&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85047689512&partnerID=8YFLogxK

U2 - 10.1016/S0042-6822(03)00138-7

DO - 10.1016/S0042-6822(03)00138-7

M3 - Article

VL - 310

SP - 280

EP - 286

JO - Virology

JF - Virology

SN - 0042-6822

IS - 2

ER -