Linked Life Data

12700132

Source:http://linkedlifedata.com/resource/pubmed/id/12700132

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2003-4-17
pubmed:abstractText
Focal adhesion kinase (FAK) was first described in 1992 as a novel nonreceptor protein-tyrosine kinase localized prominently within focal adhesions, suggesting a signaling role in regulating cell behavior resulting from integrin interaction with the extracellular matrix. Subsequent studies over the past decade have established functional roles for FAK as a positive regulator of both cell motility and cell survival, while providing considerable insight into signaling mechanisms involved. FAK signaling results from its ability to become highly phosphorylated in response to integrin-mediated adhesion on Tyr-397, permitting interactions with a number of different signaling effectors containing Src homology 2 (SH2) domains. Src-family kinases recruited to the Tyr-397 site phosphorylate two FAK-interacting proteins, Crk-associated substrate (CAS) and paxillin, which results ultimately in regulation of Rho-family GTPases contributing to cell motility. CAS phosphorylation, as well as phosphatidylinositol 3-kinase (PI3K) activation resulting from its binding to the FAK Tyr-397 site, have been implicated as downstream FAK signaling events that confer a resistance to apoptosis. This article reviews these and other aspects of FAK signaling and function.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1093-4715
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
d982-96
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Focal adhesion kinase signaling activities and their implications in the control of cell survival and motility.
pubmed:affiliation
Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. steve.hanks@vanderbilt.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review