RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/29056325http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29056325http://www.w3.org/2000/01/rdf-schema#comment"The PI3K signaling pathway regulates cell growth and movement and is heavily mutated in cancer. Class I PI3Ks synthesize the lipid messenger PI(3,4,5)P3. PI(3,4,5)P3 can be dephosphorylated by 3- or 5-phosphatases, the latter producing PI(3,4)P2. The PTEN tumor suppressor is thought to function primarily as a PI(3,4,5)P3 3-phosphatase, limiting activation of this pathway. Here we show that PTEN also functions as a PI(3,4)P2 3-phosphatase, both in vitro and in vivo. PTEN is a major PI(3,4)P2 phosphatase in Mcf10a cytosol, and loss of PTEN and INPP4B, a known PI(3,4)P2 4-phosphatase, leads to synergistic accumulation of PI(3,4)P2, which correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated cells. PTEN deletion increased PI(3,4)P2 levels in a mouse model of prostate cancer, and it inversely correlated with PI(3,4)P2 levels across several EGF-stimulated prostate and breast cancer lines. These results point to a role for PI(3,4)P2 in the phenotype caused by loss-of-function mutations or deletions in PTEN."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2017.09.024"xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Le Novere N."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Sasaki T."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Nakanishi H."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Clark J."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Sasaki J."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Hawkins P.T."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Kielkowska A."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Niewczas I."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Stephens L.R."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Imbert M."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Eguchi S."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Anderson K.E."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Koizumi A."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Beinke S."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Habuchi T."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Pir P."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Gray A."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Barneda D."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Spensberger D."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Malek M."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Juvin V."xsd:string
http://purl.uniprot.org/citations/29056325http://purl.uniprot.org/core/author"Cosulich S."xsd:string