Linked Life Data

19590405

Source:http://linkedlifedata.com/resource/pubmed/id/19590405

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2009-8-27
pubmed:abstractText
A family of histone deacetylases (HDACs) mediates chromatin remodeling, and repression of gene expression. Deacetylation of histones within the HIV-1 long terminal repeat (LTR) by HDACs plays a key role in the maintenance of latency, whereas acetylation of histones about the LTR is linked to proviral expression and escape of HIV from latency. Global HDAC inhibition may adversely affect host gene expression, leading to cellular toxicities. Potent inhibitors selective for HDACs that maintain LTR repression could be ideal antilatency therapeutics.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1473-5571
pubmed:author
pubmed:copyrightInfo
2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1799-806
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Expression of latent human immunodeficiency type 1 is induced by novel and selective histone deacetylase inhibitors.
pubmed:affiliation
Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 7599-7435, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural