BROWSE

Related Researcher

Author's Photo

Park, Jiyoung
Molecular Metabolism Laboratory (MML)
Research Interests
  • Obesity, diabetes, adipose tissue, cancer, cancer-associated adipocyte, dermal adipocyte, metabolic memory

ITEM VIEW & DOWNLOAD

Tat-dependent repression of human immunodeficiency virus type 1 long terminal repeat promoter activity by fusion of cellular transcription factors

Cited 0 times inthomson ciCited 0 times inthomson ci
Title
Tat-dependent repression of human immunodeficiency virus type 1 long terminal repeat promoter activity by fusion of cellular transcription factors
Author
Zhao, CYChen, YLPark, JiyoungKim, JBTang, H
Keywords
HIV-1 GENE-EXPRESSION; LTR PROMOTER; HISTONE ACETYLTRANSFERASE; REGULATORY ELEMENT; PROTEIN; ACTIVATION; ELONGATION; RNA; COMPLEX; CELLS
Issue Date
2004-09
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.322, no.2, pp.614 - 622
Abstract
Transcription initiation from HIV-1 long terminal repeat (LTR) promoter requires the virally encoded transactivator, Tat, and several cellular co-factors to accomplish the Tat-dependent processive transcription elongation. Individual cellular transcription activators, LBP-1b and Oct-1, on the other hand, have been shown to inhibit LTR promoter activities probably via competitive binding against TFIID to the TATA-box in LTR promoter. To explore the genetic interference strategies against the viral replication, we took advantage of the existence of the bipartite DNA binding domains and the repression domains of LBP-1b and Oct-1 factors to generate a chimeric transcription repressor. Our results indicated that the fusion protein of LBP-1b and Oct-1 exhibited higher DNA binding affinity to the viral promoter than the individual factors, and little interference with the host cell gene expression due to its anticipated rare cognate DNA sites in the host cell genome. Moreover, the chimera exerted increased Tat-dependent repression of transcription initiation at the LTR promoter both in vitro and in vivo compared to LBP-1b, Oct-1 or combination of LBP-1b and Oct-1. These results might provide the lead in generating a therapeutic reagent useful to suppress HIV-1 replication.
URI
Go to Link
DOI
10.1016/j.bbrc.2004.07.165
ISSN
0006-291X
Appears in Collections:
BME_Journal Papers
Files in This Item:
2-s2.0-6044236980.pdf Download

find_unist can give you direct access to the published full text of this article. (UNISTARs only)

Show full item record

qrcode

  • mendeley

    citeulike

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

MENU