NDLI: Characterization of the minute virus of mice P38 core promoter elements.

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Expression status of Tax protein in human T-cell leukemia virus type 1-transformed MT4 cells: recall of MT4 cells distributed by the NIH AIDS Research and Reference Reagent Program.

Transformation and tumorigenic properties of a mutant polyomavirus containing a middle T antigen defective in Shc binding.

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The potent enhancer activity of the polycythemic strain of spleen focus-forming virus in hematopoietic cells is governed by a binding site for Sp1 in the upstream control region and by a unique enhancer core motif, creating an exclusive target for PEBP/CBF.

Evolution of the human immunodeficiency virus type 1 subtype-specific V3 domain is confined to a sequence space with a fixed distance to the subtype consensus.

Nuclear import, virion incorporation, and cell cycle arrest/differentiation are mediated by distinct functional domains of human immunodeficiency virus type 1 Vpr.

pol gene diversity of five human immunodeficiency virus type 1 subtypes: evidence for naturally occurring mutations that contribute to drug resistance, limited recombination patterns, and common ancestry for subtypes B and D.

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In vitro study of the NS2-3 protease of hepatitis C virus.

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Shared usage of the chemokine receptor CXCR4 by the feline and human immunodeficiency viruses.

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Mapping promoter regions that are hypersensitive to methylation-mediated inhibition of transcription: application of the methylation cassette assay to the Epstein-Barr virus major latency promoter.

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Cyclin-dependent kinase regulation of the replication functions of polyomavirus large T antigen.

Inhibition of human immunodeficiency virus type 1 replication in vitro by a novel combination of anti-Tat single-chain intrabodies and NF-kappa B antagonists.

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Identification of GB virus C variants by phylogenetic analysis of 5'-untranslated and coding region sequences.

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Characterization of the minute virus of mice P38 core promoter elements.

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Binding of SP1 to the immediate-early protein-responsive element of the human cytomegalovirus DNA polymerase promoter.

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Sequence variation within a nonstructural region of the hepatitis G virus genome.

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cis elements that contribute to geminivirus transcriptional regulation and the efficiency of DNA replication.

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Functional interactions between monomers of the retroviral envelope protein complex.

Mutations in the N-terminal domain of human immunodeficiency virus type 1 nucleocapsid protein affect virion core structure and proviral DNA synthesis.

Induction of tumor necrosis factor alpha in human neuronal cells by extracellular human T-cell lymphotropic virus type 1 Tax.

Multimerization of polyomavirus middle-T antigen.

Mutational analysis of the adeno-associated virus type 2 Rep68 protein helicase motifs.

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Characterization of the minute virus of mice P38 core promoter elements.

Content Provider	PubMed Central
Author	Lorson, C. Pintel, D. J.
Abstract	While the minute virus of mice (MVM) P4 promoter, which drives the viral nonstructural genes, is highly active in the absence of viral proteins, P38, the capsid gene promoter, is strictly dependent on the viral nonstructural protein NS1. Once fully transactivated, however, P38 mediates twice the steady-state level of expression achieved by P4. In this report, we address the discrepancy between the ability of P38 to mediate very high levels of activated transcription yet only low levels of basal expression, and we investigate the determinants that govern P38 basal expression. The isolated P38 core promoter elements (the P38 Sp1-binding site and TATA element) are at least as transcriptionally competent as the analogous P4 promoter elements. Proximally positioning P4 enhancer factor-binding sequences (nucleotides [nt] 57 to 157) upstream of isolated P38 core transcription regulatory elements or upstream of a native, though abbreviated, P38 cassette (MVM nt 1938 to 2072) confers significant levels of expression to P38 in the absence of NS1, while the full left-end hairpin sequences (nt 1 to 133) elevate basal P38 activity to levels equivalent to P4 basal levels. In the context of the complete viral genome, however, proximally positioned enhancer sequences are unable to confer significant levels of expression to P38, suggesting that low P38 basal levels are a consequence not only of a lack of proximal enhancer elements but also of additional positional regulatory constraints which can be overcome by NS1.
Starting Page	6568
File Format	PDF
ISSN	10985514
e-ISSN	10985514
Journal	Journal of Virology
Issue Number	9
Volume Number	71
Language	English
Publisher Date	1997-09-01
Access Restriction	Open
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Virology Immunology Microbiology Insect Science

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