Skip to content Skip to navigation
University of Warwick
  • Study
  • |
  • Research
  • |
  • Business
  • |
  • Alumni
  • |
  • News
  • |
  • About

University of Warwick
Publications service & WRAP

Highlight your research

  • WRAP
    • Home
    • Search WRAP
    • Browse by Warwick Author
    • Browse WRAP by Year
    • Browse WRAP by Subject
    • Browse WRAP by Department
    • Browse WRAP by Funder
    • Browse Theses by Department
  • Publications Service
    • Home
    • Search Publications Service
    • Browse by Warwick Author
    • Browse Publications service by Year
    • Browse Publications service by Subject
    • Browse Publications service by Department
    • Browse Publications service by Funder
  • Help & Advice
University of Warwick

The Library

  • Login
  • Admin

TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-1-BETA INDUCE SPECIFIC SUBUNITS OF NF-KAPPAB TO BIND THE HIV-1 ENHANCER - CHARACTERIZATION OF TRANSCRIPTION FACTORS CONTROLLING HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GENE-EXPRESSION IN NEURAL CELLS

Tools
- Tools
+ Tools

UNSPECIFIED (1994) TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-1-BETA INDUCE SPECIFIC SUBUNITS OF NF-KAPPAB TO BIND THE HIV-1 ENHANCER - CHARACTERIZATION OF TRANSCRIPTION FACTORS CONTROLLING HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GENE-EXPRESSION IN NEURAL CELLS. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 203 (1). pp. 623-630.

Research output not available from this repository, contact author.

Request Changes to record.

Abstract

In human astrocytoma and neuroblastoma cell lines tumour necrosis factor alpha (TNF alpha) and interleukin 1 beta (IL-1 beta) induced NFKB and an additional KB-specific protein of approximately 80 K to bind the HIV-1 enhancer. One nucleoprotein complex contained prototypical NFKB comprising of p50 and p65 subunits and a second contained the p65 subunit and an 80 K factor, p80. Over a 24 hr period of cytokine stimulation the p50/p65 complex of NFKB was present in the nucleus whilst the second complex declined in abundance after two hours due to the decline of p80. In unstimulated cells, DNAse I footprinting revealed a previously unidentified octamer-like binding site in the negative regulatory element (NRE) of the HIV-1 long terminal repeat (LTR) which specifically bound protein factors present in human astrocytoma, neuroblastoma and murine oligodendroglioma cell lines. A second unique motif, also in the NRE, was observed with extracts from one human neuroblastoma cell line and a murine oligodendroglioma. Footprinting analysis also confirmed that Sp1, TATA, Site A and Site B motifs of the LTR were occupied by nuclear factors present in neural cells (C) 1994 Academic Press, Inc.

Item Type: Journal Article
Subjects: Q Science > QD Chemistry
Q Science > QH Natural history > QH301 Biology
Journal or Publication Title: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Publisher: ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
ISSN: 0006-291X
Official Date: 30 August 1994
Dates:
DateEvent
30 August 1994UNSPECIFIED
Volume: 203
Number: 1
Number of Pages: 8
Page Range: pp. 623-630
Publication Status: Published

Data sourced from Thomson Reuters' Web of Knowledge

Request changes or add full text files to a record

Repository staff actions (login required)

View Item View Item
twitter

Email us: wrap@warwick.ac.uk
Contact Details
About Us