Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1997-1-7
pubmed:abstractText
The HIV-1 Tat protein transactivates HIV, viral and some host cell genes. Tat can be released by infected cells and acts extracellularly in the microenvironment, regulating functions of immunocompetent and mesenchymal cells. One of the most striking effects of Tat is the induction of a functional program in vascular cells related to angiogenesis and inflammation (migration, proliferation and expression of plasminogen activator inhibitor-1 and E selectin). Tat induces growth of Kaposi's sarcoma (KS) spindle cells and is angiogenic in vivo and in transgenic mice10-12. We previously reported that Tat is a direct angiogenic factor and noted the Tat arginine- and lysine-rich sequence is similar to that of other potent angiogenic growth factors, such as vascular endothelial growth factor-A (VEGF-A). It is possible that Tat mimics one of these factors by interacting with its growth factor tyrosine kinase receptor. Here we demonstrate that Tat specifically binds and activates the Flk-1/kinase insert domain receptor (Flk-1/KDR), a VEGF-A tyrosine kinase receptor (for review see ref. 13), and that Tat-induced angiogenesis is blocked by agents blocking the Flk-1/KDR receptor. Endothelial cell stimulation by Tat occurs in the absence of activation of FLT-1, another VEGF-A tyrosine kinase receptor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Collagen, http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations, http://linkedlifedata.com/resource/pubmed/chemical/Endothelial Growth Factors, http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, tat, http://linkedlifedata.com/resource/pubmed/chemical/Laminin, http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines, http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans, http://linkedlifedata.com/resource/pubmed/chemical/Receptor Protein-Tyrosine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Growth Factor, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Vascular Endothelial..., http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A, http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factors, http://linkedlifedata.com/resource/pubmed/chemical/matrigel, http://linkedlifedata.com/resource/pubmed/chemical/tat Gene Products, Human...
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1078-8956
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1371-5
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:8946838-Animals, pubmed-meshheading:8946838-Binding Sites, pubmed-meshheading:8946838-COS Cells, pubmed-meshheading:8946838-Chemotaxis, pubmed-meshheading:8946838-Collagen, pubmed-meshheading:8946838-Drug Combinations, pubmed-meshheading:8946838-Endothelial Growth Factors, pubmed-meshheading:8946838-Endothelium, Vascular, pubmed-meshheading:8946838-Enzyme Activation, pubmed-meshheading:8946838-Gene Products, tat, pubmed-meshheading:8946838-HIV-1, pubmed-meshheading:8946838-Humans, pubmed-meshheading:8946838-Laminin, pubmed-meshheading:8946838-Lymphokines, pubmed-meshheading:8946838-Neovascularization, Pathologic, pubmed-meshheading:8946838-Phosphorylation, pubmed-meshheading:8946838-Proteoglycans, pubmed-meshheading:8946838-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:8946838-Receptors, Growth Factor, pubmed-meshheading:8946838-Receptors, Vascular Endothelial Growth Factor, pubmed-meshheading:8946838-Vascular Endothelial Growth Factor A, pubmed-meshheading:8946838-Vascular Endothelial Growth Factors, pubmed-meshheading:8946838-tat Gene Products, Human Immunodeficiency Virus
pubmed:year
1996
pubmed:articleTitle
The angiogenesis induced by HIV-1 tat protein is mediated by the Flk-1/KDR receptor on vascular endothelial cells.
pubmed:affiliation
Dipartimento di Genetica, Biologia e Chimica Medica, Università di Torino, Turin, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't