PMID- 7929236
OWN - NLM
STAT- MEDLINE
DCOM- 19941117
LR  - 20210212
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 269
IP  - 41
DP  - 1994 Oct 14
TI  - Repression of transforming growth factor beta 1 promoter by the adenovirus 
      oncogene E1A. Identification of a unique GC-rich sequence as a target for E1A 
      repression.
PG  - 25392-9
AB  - The transforming growth factor beta 1 (TGF-beta 1) is a key regulator of 
      proliferation and differentiation in a wide variety of cell types. It is a potent 
      growth inhibitor for most epithelial, endothelial, lymphoid, and myeloid cells. 
      In the present study, we showed that a DNA virus oncoprotein, E1A, strongly 
      repressed the activity of the TGF-beta 1 promoter in a variety of cell lines. 
      Interestingly, this repression was specific for 12 S E1A because 13 S E1A was 
      much less active in this assay. Analysis of a series of E1A mutants showed that 
      the repression was dependent on the amino terminus and the conserved region 1 of 
      the E1A protein. To identify the target sequence for E1A repression in the 
      TGF-beta 1 promoter, a series of mutant promoters were analyzed and a 10-base 
      pair GC-rich sequence between -91 and -82 was found to be the major target for 
      E1A repression of the promoter. Using chimeric reporter constructs, we provide 
      evidence that the 10-base pair GC-rich sequence is sufficient to impart 
      sequence-specific E1A repression to a heterologous promoter. Additionally, we 
      suggest that the mechanism of E1A repression through this GC-rich element does 
      not involve abrogation of the retinoblastoma control of the TGF-beta 1 promoter.
FAU - Datta, P K
AU  - Datta PK
AD  - Center for Molecular Biology of Oral Diseases, College of Dentistry (M/C 860), 
      University of Illinois, Chicago 60612.
FAU - Bagchi, S
AU  - Bagchi S
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Adenovirus E1A Proteins)
RN  - 0 (Adenovirus E2 Proteins)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Transforming Growth Factor beta)
RN  - EC 2.3.1.28 (Chloramphenicol O-Acetyltransferase)
SB  - IM
MH  - Adenovirus E1A Proteins/*genetics
MH  - Adenovirus E2 Proteins/genetics
MH  - Animals
MH  - Base Sequence
MH  - Binding Sites
MH  - Cells, Cultured
MH  - Chloramphenicol O-Acetyltransferase/biosynthesis/genetics
MH  - Conserved Sequence
MH  - DNA Mutational Analysis
MH  - Gene Expression
MH  - *Gene Expression Regulation
MH  - Genes, Reporter
MH  - Humans
MH  - Mice
MH  - Mink
MH  - Molecular Sequence Data
MH  - Oncogenes/*genetics
MH  - Promoter Regions, Genetic/*genetics
MH  - Protein Binding
MH  - Recombinant Fusion Proteins/biosynthesis
MH  - Species Specificity
MH  - Transcription, Genetic
MH  - Transforming Growth Factor beta/biosynthesis/*genetics
EDAT- 1994/10/14 00:00
MHDA- 1994/10/14 00:01
CRDT- 1994/10/14 00:00
PHST- 1994/10/14 00:00 [pubmed]
PHST- 1994/10/14 00:01 [medline]
PHST- 1994/10/14 00:00 [entrez]
AID - S0021-9258(18)47262-6 [pii]
PST - ppublish
SO  - J Biol Chem. 1994 Oct 14;269(41):25392-9.