Linked Life Data

21029719

Source:http://linkedlifedata.com/resource/pubmed/id/21029719

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-1-10
pubmed:abstractText
Human immunodeficiency virus (HIV) regulatory protein Tat has pro-oxidant property, which might contribute to Tat-induced long terminal repeat region (LTR) transactivation. However, the intracellular mechanisms whereby Tat triggers ROS production, and the relationship between Tat-induced ROS production and LTR transactivation, are still subject to debate. The present study was undertaken to evaluate the specific effects of Tat on nicotinamide adenine denucleotide phosphate (NADPH) oxidase in MAGI cells, and to determine the specific role of NADPH oxidase in Tat-induced LTR transactivation. Application of Tat to MAGI cells caused increases in ROS formation that were prevented by both pharmacologic NADPH oxidase inhibitors and by siRNA Nox2, but not by other inhibitors of pro-oxidant enzymes or siRNA Nox4. Furthermore, inhibition of NADPH oxidase by both pharmacologic NADPH oxidase inhibitors and by siRNA Nox2 attenuated Tat-induced p65 phosphorylation and IKK phosphorylation. Phosphatidylinositol 3-kinase/Akt signaling pathway was involved in Tat-induced NADPH oxidase stimulation. Finally, NADPH oxidase inhibitors or Nox2 siRNA, but not control siRNA, inhibited Tat-induced LTR transactivation. Tat-induced HIV-1 LTR transactivation was inhibited in wortmannin or LY294002 treated cells compared to control cells. Together, these data describe a specific and biologically significant signaling component of the MAGI cells response to Tat, and suggest the PI3K/Akt signaling pathway might originate in part with Tat-induced activation of NADPH oxidase and LTR transactivation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1096-0384
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
505
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
266-72
pubmed:meshHeading
pubmed-meshheading:21029719-HIV-1, pubmed-meshheading:21029719-HeLa Cells, pubmed-meshheading:21029719-Humans, pubmed-meshheading:21029719-I-kappa B Proteins, pubmed-meshheading:21029719-Membrane Glycoproteins, pubmed-meshheading:21029719-NADPH Oxidase, pubmed-meshheading:21029719-NF-kappa B, pubmed-meshheading:21029719-Oxidative Stress, pubmed-meshheading:21029719-Phosphatidylinositol 3-Kinase, pubmed-meshheading:21029719-Proto-Oncogene Proteins c-akt, pubmed-meshheading:21029719-Reactive Oxygen Species, pubmed-meshheading:21029719-Signal Transduction, pubmed-meshheading:21029719-Terminal Repeat Sequences, pubmed-meshheading:21029719-Transcription Factor RelA, pubmed-meshheading:21029719-Transcriptional Activation, pubmed-meshheading:21029719-tat Gene Products, Human Immunodeficiency Virus
pubmed:year
2011
pubmed:articleTitle
Akt/Nox2/NF-?B signaling pathway is involved in Tat-induced HIV-1 long terminal repeat (LTR) transactivation.
pubmed:affiliation
Beijing University of Technology, District of Chaoyang, China. zhanghs@bjut.edu.cn
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't