|
Basic Characteristics of Mutations
|
|
Mutation Site
|
L64A |
|
Mutation Site Sentence
|
In contrast, VprL64A was fully functional in arresting cells in G2/M phase of the cell cycle. |
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Mutation Level
|
Amino acid level |
|
Mutation Type
|
Nonsynonymous substitution |
|
Gene/Protein/Region
|
Vpr |
|
Standardized Encoding Gene
|
Vpr
|
|
Genotype/Subtype
|
HIV-1 |
|
Viral Reference
|
-
|
|
Functional Impact and Mechanisms
|
|
Disease
|
Acquired Immunodeficiency Syndrome
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
- |
|
Treatment
|
- |
|
Location
|
- |
|
Literature Information
|
|
PMID
|
9874563
|
|
Title
|
The HIV-1 virion-associated protein vpr is a coactivator of the human glucocorticoid receptor
|
|
Author
|
Kino T,Gragerov A,Kopp JB,Stauber RH,Pavlakis GN,Chrousos GP
|
|
Journal
|
The Journal of experimental medicine
|
|
Journal Info
|
1999 Jan 4;189(1):51-62
|
|
Abstract
|
The HIV-1 virion-associated accessory protein Vpr affects both viral replication and cellular transcription, proliferation, and differentiation. We report that Vpr enhances the activity of glucocorticoids in lymphoid and muscle-derived cell lines by interacting directly with the glucocorticoid receptor and general transcription factors, acting as a coactivator. Vpr contains the signature motif LXXLL also present in cellular nuclear receptor coactivators, such as steroid receptor coactivator 1 and p300/CREB-binding protein, which mediates their interaction with the glucocorticoid and other nuclear hormone receptors. A mutant Vpr molecule with disruption of this coactivator signature motif lost its ability to influence transcription of glucocorticoid-responsive genes and became a dominant-negative inhibitor of Vpr, possibly by retaining its general transcription factor-binding activities. The glucocorticoid coactivator activity of Vpr may contribute to increased tissue glucocorticoid sensitivity in the absence of hypercortisolism and to the pathogenesis of AIDS.
|
|
Sequence Data
|
-
|