Linked Life Data

15449141

Source:http://linkedlifedata.com/resource/pubmed/id/15449141

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-1-17
pubmed:abstractText
The HIV-1 accessory protein Vpr potentiates glucocorticoid (GC)-induced inhibition of a variety of immunologically important cytokines. We report the first instance of synergy between Vpr and GC in induction of a T cell cytokine, one which may underlie a metabolic complication of HIV infection. Accelerated bone resorption is an important complication of HIV disease and its treatment. Receptor of activated NF-kappaB ligand (RANKL) is the final effector of osteoclast differentiation and bone resorption. It is induced by exogenous GC, a prominent cofactor in bone mineral loss, as well as by elevated levels of endogenous GC, found in many patients with HIV disease. We document Vpr-mediated upregulation of RANKL, the dependence of this effect on GC receptor integrity, its function through a classic GC receptor motif, and its independence from Vpr-mediated G(2) cell cycle arrest. These data suggest a positive regulatory role for Vpr in transcriptional control of a cytokine that may be critical to one metabolic complication of HIV.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0304-8608
pubmed:author
pubmed:issnType
Print
pubmed:volume
150
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
67-78
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
HIV-1 Vpr enhances production of receptor of activated NF-kappaB ligand (RANKL) via potentiation of glucocorticoid receptor activity.
pubmed:affiliation
Laboratory for AIDS Virus Research, Department of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't