Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2006-8-2
pubmed:abstractText
PTEN, one of the most frequently mutated genes in human cancer, acts as a tumor suppressor by dephosphorylating the plasma membrane lipid second messenger phosphoinositide-3,4,5-trisphosphate (PIP3) generated by the action of PI3Kinases. PTEN activity to prevent elevated levels of PIP3 and tumorigenesis depends on its interaction with the lipid bilayer. PTEN binds dynamically to the plasma membrane through a complex mix of protein-lipid and protein-protein interactions and the translocation is regulated by several mechanisms including C-terminal tail phosphorylations. Here we have summarized our current view of the interaction of PTEN with the plasma membrane and what the implications are for cancer biology.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1523-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Regulation of PTEN function as a PIP3 gatekeeper through membrane interaction.
pubmed:affiliation
Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. fvazquez@jhmi.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, N.I.H., Extramural