PMID- 8474178
OWN - NLM
STAT- MEDLINE
DCOM- 19930517
LR  - 20200724
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 67
IP  - 5
DP  - 1993 May
TI  - Sequences downstream of the RNA initiation site regulate human T-cell 
      lymphotropic virus type I basal gene expression.
PG  - 2894-902
AB  - Sequences which control basal human T-cell lymphotropic virus type I (HTLV-I) 
      transcription probably play an important role in initiation and maintenance of 
      virus replication. We have identified and analyzed a 45-nucleotide sequence 
      (downstream regulatory element 1 [DRE 1]) at the boundary of the R/U5 region of 
      the long terminal repeat which is required for HTLV-I basal transcription. The 
      basal promoter strength of constructs that contained deletions in the R/U5 region 
      of the HTLV-I long terminal repeat were analyzed by chloramphenicol 
      acetyltransferase assays following transfection of Jurkat T cells. We 
      consistently observed a 10-fold decrease in basal promoter activity when 
      sequences between +202 to +246 were deleted. By reverse transcriptase polymerase 
      chain reaction RNA analysis, we confirmed that the drop in chloramphenicol 
      acetyltransferase activity was paralleled by a decrease in the level of 
      steady-state RNA. DRE 1 did not affect the level of Tax1 transactivation. Using a 
      gel shift assay, we have purified a highly enriched fraction that could 
      specifically bind DRE 1. This DNA affinity column fraction contained four 
      detectable proteins on sodium dodecyl sulfate (SDS)-polyacrylamide gel 
      electrophoresis: p37, p50, p60, and p100. The affinity column fraction stimulated 
      HTLV-I transcription approximately 12-fold in vitro. No effect was observed with 
      the human immunodeficiency virus or adenovirus major late promoters. Following 
      renaturation of the proteins isolated from an SDS-containing gel, p37, but not 
      the other protein fractions, was able to specifically bind to DRE 1.
FAU - Kashanchi, F
AU  - Kashanchi F
AD  - Laboratory of Molecular Virology, National Cancer Institute, Bethesda, Maryland 
      20892.
FAU - Duvall, J F
AU  - Duvall JF
FAU - Lindholm, P F
AU  - Lindholm PF
FAU - Radonovich, M F
AU  - Radonovich MF
FAU - Brady, J N
AU  - Brady JN
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Recombinant Proteins)
RN  - EC 2.3.1.28 (Chloramphenicol O-Acetyltransferase)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chloramphenicol O-Acetyltransferase/biosynthesis
MH  - Chromatography, Affinity
MH  - DNA Mutational Analysis
MH  - DNA-Binding Proteins/isolation & purification/*metabolism
MH  - *Gene Expression Regulation, Viral
MH  - Human T-lymphotropic virus 1/*genetics
MH  - Molecular Sequence Data
MH  - Nuclear Proteins/isolation & purification/metabolism
MH  - Polymerase Chain Reaction
MH  - Recombinant Proteins/biosynthesis
MH  - Regulatory Sequences, Nucleic Acid/*genetics
MH  - Sequence Deletion
MH  - T-Lymphocytes/cytology
MH  - *Transcription, Genetic
PMC - PMC237615
EDAT- 1993/05/01 00:00
MHDA- 1993/05/01 00:01
PMCR- 1993/05/01
CRDT- 1993/05/01 00:00
PHST- 1993/05/01 00:00 [pubmed]
PHST- 1993/05/01 00:01 [medline]
PHST- 1993/05/01 00:00 [entrez]
PHST- 1993/05/01 00:00 [pmc-release]
AID - 10.1128/JVI.67.5.2894-2902.1993 [doi]
PST - ppublish
SO  - J Virol. 1993 May;67(5):2894-902. doi: 10.1128/JVI.67.5.2894-2902.1993.