Document 0423
 DOCN  M9650423
 TI    Essential role of NF-kappa B in transactivation of the human
       immunodeficiency virus long terminal repeat by the human cytomegalovirus
       1E1 protein.
 DT    9605
 AU    Kim S; Yu SS; Kim VN; Institute for Molecular Biology and Genetics,
       Seoul National; University, Kwan-Ak-Gu, Korea.
 SO    J Gen Virol. 1996 Jan;77 ( Pt 1):83-91. Unique Identifier : AIDSLINE
       MED/96145137
 AB    The 72 kDa 1E1 protein of human cytomegalovirus (HCMV) is one of a few
       viral regulatory proteins expressed immediately after infection of a
       host cell. Although it is now well-established that 1E1 is a potent
       transcriptional activator of the human immunodeficiency virus (HIV) long
       terminal repeat (LTR), the identity of the nucleotide sequence
       responsive to 1E1 remains elusive and the molecular mechanism of this
       interaction is not well-understood. We have constructed various LTR
       mutants and tested them for their ability to be activated by 1E1 using
       transient transfection assays. Mutations in the NF-kappa B sites, of
       either a few changes in the nucleotide sequence or a deletion of the
       entire region, abrogated 1E1-driven transactivation. Deletion of the
       Tat-responsive element (TAR) had no significant effect on reporter
       expression. Mutations in the Sp1 sites or the TATA box significantly
       lowered LTR activity, but this is probably due to an effect on the
       general transcription system, as these elements are also required for
       the transactivation of the LTR by many stimulators including Tat, tumour
       necrosis factor alpha (TNF-alpha). E1A/E1B and phorbol myristate acetate
       (PMA). In addition, gel retardation analysis demonstrated that NF- kappa
       B activity was significantly increased in human T lymphoid H9 and
       monocytic U937 cell lines constitutively expressing 1E1. Taken together,
       these data suggest that NF- kappa B plays a central role in the 1E1
       transactivation of the HIV LTR.
 DE    Base Sequence  Cell Line  Down-Regulation (Physiology)  Gene Expression
       Regulation, Viral  Genetic Vectors  Hela Cells  Human  HIV/*GENETICS
       HIV Long Terminal Repeat/*GENETICS  Immediate-Early
       Proteins/GENETICS/*METABOLISM  Molecular Sequence Data  NF-kappa
       B/GENETICS/*METABOLISM  Regulatory Sequences, Nucleic Acid  Sequence
       Deletion  Support, Non-U.S. Gov't  *Trans-Activation (Genetics)
       Transcription, Genetic  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).