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1994-08-20
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Document 0475
DOCN M9480475
TI Oncostatin M activates phosphatidylinositol-3-kinase in Kaposi's sarcoma
cells.
DT 9410
AU Soldi R; Graziani A; Benelli R; Ghigo D; Bosia A; Albini A; Bussolino F;
Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy.
SO Oncogene. 1994 Aug;9(8):2253-60. Unique Identifier : AIDSLINE
MED/94309900
AB Oncostatin M (OM) is a polypeptide cytokine that induces autocrine and
paracrine effects on AIDS-Kaposi's sarcoma (KS) cells (Nair et al.,
Science, 255, 1430-1432, 1992; Miles et al., Science, 255, 1432-1434,
1992). The signalling pathways underlying this activation are largely
unknown. We have found that OM binding to KS cell lines in vitro
identifies a higher affinity binding site (Kd 10-20 pM) with a lower
affinity (Kd 1.5 nM), high capacity binding site. The binding of OM to
its receptor at the KS cell surface stimulates a rapid tyrosine
phosphorylation of multiple proteins, including the p85 regulatory
subunit of phosphatidylinositol-3-kinase (PI3K). In addition OM can
stimulate the in vivo activation of PI3K and increases the PI3K activity
in anti-phosphotyrosine and anti-src kinase family antibody directed
immunoprecipitates. Genistein, an inhibitor of tyrosine kinases,
inhibits the synthesis of phosphatidylinositol 3,4-biphosphate and the
growth of KS cells. Finally, OM enhances tyrosine kinase activity in
immune complex kinase assay performed with antibody anti-src kinase
family. These data suggest that in KS cells OM can stimulate formation
of tyrosine kinase co-ordinate signalling complexes, containing at least
src kinase family and PI3K, which can drive the accumulation of the
putative second-messengers D3-phosphorylated phosphoinositides.
DE Antineoplastic Agents/*PHARMACOLOGY Cytokines/*PHARMACOLOGY Human
Peptides/*PHARMACOLOGY Phosphatidylinositols/METABOLISM
Phosphorylation Phosphotransferases (Alcohol Group
Acceptor)/*METABOLISM Protein-Tyrosine Kinase/METABOLISM Sarcoma,
Kaposi's/*ENZYMOLOGY Support, Non-U.S. Gov't Tumor Cells, Cultured
Tyrosine/METABOLISM JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).