Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
45
pubmed:dateCreated
1997-12-12
pubmed:abstractText
Leukocytes and platelets require stimulation for optimal beta3 integrin receptor function, whereas beta3 function is constitutive in many other cells. The molecular mechanisms that enhance integrin function in stimulated hematopoietic cells are poorly understood. Phosphorylation of the beta3 cytoplasmic tail is a recently described but prevalent phenomenon, with unknown effects on alphavbeta3 function. Here, we show that mutation of the beta3 cytoplasmic tail tyrosine 747 to phenylalanine (Y747F) prevents beta3 tyrosine phosphorylation in two cell lines. Whereas this mutation has no effect on alphavbeta3-mediated adhesion in a cell with constitutive beta3 function, it completely abolishes adhesion and clot retraction by a cell that requires stimulation for beta3 function. Ligand-induced conformational change as detected by LIBS-1 antibody occurs normally in Y747F mutant alphavbeta3. Thus, tyrosine 747 of beta3 is required for stimulation of alphavbeta3-mediated adhesion, probably due to its phosphorylation. Because the motif in beta3 required for tyrosine phosphorylation is shared by several integrin beta-chains, this may be a conserved mechanism for regulation of integrin-dependent adhesion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
272
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
28757-61
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Requirement of integrin beta3 tyrosine 747 for beta3 tyrosine phosphorylation and regulation of alphavbeta3 avidity.
pubmed:affiliation
Department of Medicine, Infectious Diseases Division, Washington University School of Medicine, St. Louis, Missouri 63110, USA. blystone@id.wustl.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't