A novel T-cell protein which recognizes a palindromic sequence in the negative regulatory element of the human immunodeficiency virus long terminal repeat.
Two major protein-binding sites within the negative regulatory element of the human immunodeficiency virus type 1 long terminal repeat have been identified. One (site B) contained a palindromic sequence with homology to steroid/thyroid hormone response elements but was distinct from previously described binding sites of this class. A novel T-cell protein recognized the palindromic sequence within site B and also bound estrogen- or thyroid hormone-response elements with lower affinity. A 7-base-pair mutation in the site B palindrome, which destroyed protein binding, resulted in increased expression from the human immunodeficiency virus type 1 long terminal repeat in T cells.
Orchard
K
K
Institute of Cancer Research, Chester Beatty Laboratories, London, England.
Perkins
N
N
Chapman
C
C
Harris
J
J
Emery
V
V
Goodwin
G
G
Latchman
D
D
Collins
M
M
D001483:Base Sequence; D002460:Cell Line; D004252:DNA Mutational Analysis; D004268:DNA-Binding Proteins / Q000502:physiology*; D015967:Gene Expression Regulation, Viral; D015497:HIV-1 / Q000235:genetics*; D006801:Humans; D066298:In Vitro Techniques; D008745:Methylation; D008969:Molecular Sequence Data; D009687:Nuclear Proteins / Q000502:physiology*; D012045:Regulatory Sequences, Nucleic Acid; D012091:Repetitive Sequences, Nucleic Acid; D012097:Repressor Proteins / Q000502:physiology; D013601:T-Lymphocytes / Q000382:microbiology*
D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D012097:Repressor Proteins