Linked Life Data

10764760

Source:http://linkedlifedata.com/resource/pubmed/id/10764760

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
27
pubmed:dateCreated
2000-8-16
pubmed:abstractText
To study the role of MAPK cascades in the regulation of naturally occurring human immunodeficiency virus type 1 long terminal repeats (HIV-1 LTRs), we analyzed several HIV-1 LTRs from patients at different stages of disease progression. One of these naturally occurring HIV-1 LTRs contains an insertion termed the most frequent naturally occurring length polymorphism (MFNLP) and exhibited high inducibility upon T cell activation. We found that the protein kinase mixed lineage kinase 3/src-homology 3 domain-containing proline-rich kinase, a specific activator of the stress-activated protein kinase (SAPK)/JNK signaling pathway in T lymphocytes, induces high transcriptional activation of this promoter. Promoter inducibility is inhibited by the SAPK/JNK inhibitor, the JNK binding domain of the JNK interacting protein 1, and Tam-67 (N-terminal deletion mutant of c-Jun). In electrophoretic mobility shift assay, several protein complexes were found to bind to the MFNLP sequence in T cells. We identified AP-1 factors c-Fos and JunB as MFNLP-binding proteins, whose binding is abolished by introducing point mutations in the 3'-half of the MFNLP sequence. Introduction of these point mutations into the MFNLP containing HIV-1 LTR reduced src-homology 3 domain-containing proline-rich kinase -mediated transactivation. These data indicate that the AP-1-like binding site in the MFNLP sequence gives rise to a higher inducibility of natural HIV-LTRs by the SAPK/JNK signaling pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
275
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
20382-90
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10764760-Binding, Competitive, pubmed-meshheading:10764760-Binding Sites, pubmed-meshheading:10764760-DNA-Binding Proteins, pubmed-meshheading:10764760-HIV Long Terminal Repeat, pubmed-meshheading:10764760-HIV-1, pubmed-meshheading:10764760-Humans, pubmed-meshheading:10764760-JNK Mitogen-Activated Protein Kinases, pubmed-meshheading:10764760-MAP Kinase Kinase Kinases, pubmed-meshheading:10764760-Mitogen-Activated Protein Kinases, pubmed-meshheading:10764760-Mutation, pubmed-meshheading:10764760-Oligodeoxyribonucleotides, pubmed-meshheading:10764760-Polymorphism, Genetic, pubmed-meshheading:10764760-Protein-Serine-Threonine Kinases, pubmed-meshheading:10764760-Signal Transduction, pubmed-meshheading:10764760-T-Lymphocytes, pubmed-meshheading:10764760-Transcription Factor AP-1, pubmed-meshheading:10764760-Transcriptional Activation, pubmed-meshheading:10764760-Tumor Cells, Cultured
pubmed:year
2000
pubmed:articleTitle
Transactivation of naturally occurring HIV-1 long terminal repeats by the JNK signaling pathway. The most frequent naturally occurring length polymorphism sequence introduces a novel binding site for AP-1 factors.
pubmed:affiliation
Institut für Medizinische Strahlenkunde und Zellforschung, Universität Würzburg, Versbacher Strasse 5, D-97078 Würzburg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't