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M9620234.TXT
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1996-02-26
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Document 0234
DOCN M9620234
TI Transcription factor TFIID is a direct functional target of the
adenovirus E1A transcription-repression domain.
DT 9602
AU Song CZ; Loewenstein PM; Toth K; Green M; Institute for Molecular
Virology, St. Louis University School of; Medicine, MO 63110, USA.
SO Proc Natl Acad Sci U S A. 1995 Oct 24;92(22):10330-3. Unique Identifier
: AIDSLINE MED/96036078
AB The 243-amino acid adenovirus E1A oncoprotein both positively and
negatively modulates the expression of cellular genes involved in the
regulation of cell growth. The E1A transcription repression function
appears to be linked with its ability to induce cellular DNA synthesis,
cell proliferation, and cell transformation, as well as to inhibit cell
differentiation. The mechanism by which E1A represses the transcription
of various promoters has proven enigmatic. Here we provide several lines
of evidence that the TATA-box binding protein (TBP) component of
transcription factor TFIID is a cellular target of the E1A repression
function encoded within the E1A N-terminal 80 amino acids. (i) The E1A
N-terminal 80 amino acids [E1A-(1-80)protein] efficiently represses
basal transcription from TATA-containing core promoters in vitro. (ii)
TBP reverses completely E1A repression in vitro. (iii) TBP restores
transcriptional activity to E1A-(1-80) protein affinity-depleted nuclear
extracts. (iv) The N-terminal repression domain of E1A interacts
directly and specifically with TBP in vitro. These results may help
explain how E1A represses a set of genes that lack common upstream
promoter elements.
DE Adenovirus E1A Proteins/*METABOLISM Cell Differentiation Cell Division
Cell Nucleus/METABOLISM Cell Transformation, Viral Chromatography,
Affinity DNA Primers DNA Replication DNA-Binding Proteins/METABOLISM
Hela Cells Human *HIV Long Terminal Repeat Recombinant
Proteins/METABOLISM Support, U.S. Gov't, P.H.S. Suppression, Genetic
Templates Transcription Factors/ISOLATION & PURIF/*METABOLISM
*Transcription, Genetic TATA Box JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).