The HIV long terminal repeat. NLM AIDSLINE Important note: Information in this article was accurate in 1993. The state of the art may have changed since the publication date.

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The HIV long terminal repeat.

Harvard AIDS Inst Ser; 1:391-435 1991. Unique Identifier : AIDSLINE ICDB/93686279
Anonymous; No affiliation given

Abstract: HIV-1 is subject to transcriptional regulation. The HIV promoter functions poorly in most cell types studied. For example, the HIV-1 long terminal repeat (LTR) directs a much lower level of heterologous gene expression in human CD4+ lymphocytes than does the LTR of the Rous sarcoma virus, an avian retrovirus. Sequences distal to the site of RNA initiation, located within the 5' region of the HIV LTR, contribute to the low level of activity of the HIV-1 promoter. The HIV LTR is reviewed in the following chapters: nuclear proteins implicated in HIV-1 transcriptional control (nuclear factors that bind to DNA and RNA control regions of the HIV-1 promoter), identification of a rel-related family of kappa B enhancer binding proteins (studies with v-rel oncogene with implications for the regulation of HIV-1 gene expression) and cellular transcription factors that regulate HIV-1 replication (cis-acting sequences within the negative regulatory element and cellular proteins that bind to the HIV-1 LTR upstream stimulatory factor and NFAT-1 sequences).
Keywords: Enhancer Elements (Genetics) Gene Expression Regulation, Viral Genes, Viral *HIV Long Terminal Repeat HIV-1/*GENETICS/PHYSIOLOGY Nuclear Proteins/GENETICS Transcription Factors/GENETICS Transcription, Genetic Virus Replication/GENETICS MONOGRAPHKWDenhancerelements(genetics)geneexpressionregulation,viralgenes,viralKWDhivlongterminalrepeathiv-1/KWDgenetics/physiologynuclearproteins/geneticstranscriptionfactors/geneticstranscription,geneticvirusreplication/geneticsmonograph
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M9320882

Copyright © 1993 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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