Choo, Andrew Y

Hwang, Daniel S

Madesh, Muniswamy

Muthumani, Karuppiah

Premkumar, Arumugam

Thompson, Craig B

Weiner, David B

Zong, Wei-Xing

English

PubMed

Karuppiah Muthumani

Andrew Y Choo

Wei-Xing Zong

Muniswamy Madesh

Daniel S Hwang

Arumugam Premkumar

Craig B Thompson

David B Weiner

Crossref

The HIV-1 Vpr and glucocorticoid receptor complex is a gain of function interaction that prevents the nuclear localization of PARP-1

Thompson Craig B

Premkumar Arumugam

Hwang Daniel S

Madesh Muniswamy

Zong Wei-Xing

Choo Andrew Y

Muthumani Karuppiah

Weiner David B

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Retrovirology

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Retrovirology
Open AccessOral presentation
The HIV-1 Vpr and glucocorticoid receptor complex is a gain of 
function interaction that prevents the nuclear localization of 
PARP-1
Karuppiah Muthumani*1, Andrew Y Choo1, Wei-Xing Zong2, 
Muniswamy Madesh2, Daniel S Hwang1, Arumugam Premkumar3, 
Craig B Thompson2 and David B Weiner1
Address: 1Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, 19104, 
USA, 2Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania School of Medicine, Pennsylvania, 
19104, USA and 3Laboratory of Molecular Neuropharmacology, Memorial Sloan-Kettering Cancer Center, New York, New York, 10021, USA
* Corresponding author    
The Vpr protein of HIV-1 functions as a vital accessory
gene by regulating various cellular functions including
cell differentiation, apoptosis, NF-κB suppression and cell
cycle arrest of the host cell. Several reports have suggested
that Vpr complexes with the glucocorticoid receptor (GR),
but it remains unclear whether the GR pathway is required
for Vpr's effects. Here we report that Vpr utilizes the GR
pathway as a recruitment vehicle for the NF-κB coactivat-
ing protein Poly(ADP-Ribose) Polymerase-1 (PARP-1).
The glucocorticoid receptor interaction with Vpr is both
necessary and sufficient to facilitate this interaction by
potentiating the formation of a Vpr/GR/PARP-1 complex.
The recruitment of PARP-1 by the Vpr/GR complex pre-
vents its nuclear localization, which is necessary for Vpr to
suppress NF-κB. The association of GR with PARP-1 is not
observed with steroid (glucocorticoid) treatment, suggest-
ing that the GR association with PARP-1 is a gain of func-
tion solely attributed to HIV-1 Vpr. These data provide
important insight into Vpr biology and its role in HIV
pathogenesis.
from 2006 International Meeting of The Institute of Human Virology
Baltimore, USA. 17–21 November, 2006
Published: 21 December 2006
Retrovirology 2006, 3(Suppl 1):S105 doi:10.1186/1742-4690-3-S1-S105
<supplement> <title> <p>2006 International Meeting of The Institute of Human Virology</p> </title> <note>Meeting abstracts. A single PDF containing all abstracts in this Supplement is available <a href=" http://www.biomedcentral.com/content/files/pdf/1742-4690-3-S1-full.pdf ">here</a></note> <url>http://www.biomedcentral.com/content/pdf/1742-4690-3-S1-info.pdf</url></supplement>
© 2006 Muthumani et al; licensee BioMed Central Ltd. 


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The HIV-1 Vpr and glucocorticoid receptor complex is a gain of function interaction that prevents the nuclear localization of PARP-1

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