(PDF) Interleukin-6 and Glucocorticoids Synergistically

Interleukin-6 and Glucocorticoids Synergistically Induce Human Immunodeficiency Virus Type-1 Expression in Chronically Infected U1 Cells by a Long Terminal Repeat Independent Post-Transcriptional Mechanism

Molecular Medicine - United States

doi 10.1007/bf03401957

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October 1, 2001

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Springer Science and Business Media LLC

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Amanote Research

Interleukin-6 and Glucocorticoids Synergistically Induce Human Immunodeficiency Virus Type-1 Expression in Chronically Infected U1 Cells by a Long Terminal Repeat Independent Post-Transcriptional Mechanism

Molecular Medicine - United States

doi 10.1007/bf03401957

Full Text

Abstract

Categories

Date

Authors

Publisher

Related search

Stimulation of Tat-Associated Kinase-Independent Transcriptional Elongation From the Human Immunodeficiency Virus Type-1 Long Terminal Repeat by a Cellular Enhancer

Interleukin 6 Induces Human Immunodeficiency Virus Expression in Infected Monocytic Cells Alone and in Synergy With Tumor Necrosis Factor Alpha by Transcriptional and Post-Transcriptional Mechanisms

Suppression of Human Immunodeficiency Virus Replication by Ascorbate in Chronically and Acutely Infected Cells.

Repression of Human Immunodeficiency Virus Type 1 Long Terminal Repeat-Driven Gene Expression by Binding of the Virus to Its Primary Cellular Receptor, the CD4 Molecule.

Molecular and Functional Interactions of Transcription Factor USF With the Long Terminal Repeat of Human Immunodeficiency Virus Type 1.

The Human Factors YY1 and LSF Repress the Human Immunodeficiency Virus Type 1 Long Terminal Repeat via Recruitment of Histone Deacetylase 1

Blockade of Human Immunodeficiency Virus Type 1 Production in CD4+ T Cells by an Intracellular CD4 Expressed Under Control of the Viral Long Terminal Repeat.

Defective Accessory Genes in a Human Immunodeficiency Virus Type 1-Infected Long-Term Survivor Lacking Recoverable Virus.

Interactions of Thyroid Hormone Receptor With the Human Immunodeficiency Virus Type 1 (HIV-1) Long Terminal Repeat and the HIV-1 Tat Transactivator.