| http://purl.uniprot.org/citations/10339565 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10339565 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10339565 | http://www.w3.org/2000/01/rdf-schema#comment | "To investigate the molecular basis of PTEN-mediated tumor suppression, we introduced a null mutation into the mouse Pten gene by homologous recombination in embryonic stem (ES) cells. Pten-/-ES cells exhibited an increased growth rate and proliferated even in the absence of serum. ES cells lacking PTEN function also displayed advanced entry into S phase. This accelerated G1/S transition was accompanied by down-regulation of p27(KIP1), a major inhibitor for G1 cyclin-dependent kinases. Inactivation of PTEN in ES cells and in embryonic fibroblasts resulted in elevated levels of phosphatidylinositol 3,4,5,-trisphosphate, a product of phosphatidylinositol 3 kinase. Consequently, PTEN deficiency led to dosage-dependent increases in phosphorylation and activation of Akt/protein kinase B, a well-characterized target of the phosphatidylinositol 3 kinase signaling pathway. Akt activation increased Bad phosphorylation and promoted Pten-/-cell survival. Our studies suggest that PTEN regulates the phosphatidylinositol 3,4, 5,-trisphosphate and Akt signaling pathway and consequently modulates two critical cellular processes: cell cycle progression and cell survival."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.96.11.6199"xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.96.11.6199"xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Gao J."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Gao J."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Liu X."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Liu X."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Sun H."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Sun H."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Wu H."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Wu H."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Zhang H."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Zhang H."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Mueller B."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Mueller B."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Lesche R."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Lesche R."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Li D.M."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Li D.M."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Gavrilova N."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Gavrilova N."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Liliental J."xsd:string |
| http://purl.uniprot.org/citations/10339565 | http://purl.uniprot.org/core/author | "Liliental J."xsd:string |