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Protean PTEN: form and function Waite KA; Eng CAm J Hum Genet 2002[Apr]; 70 (4): 829-44Germline mutations distributed across the PTEN tumor-suppressor gene have been found to result in a wide spectrum of phenotypic features. Originally shown to be a major susceptibility gene for both Cowden syndrome (CS), which is characterized by multiple hamartomas and an increased risk of breast, thyroid, and endometrial cancers, and Bannayan-Riley-Ruvalcaba syndrome, which is characterized by lipomatosis, macrocephaly, and speckled penis, the PTEN hamartoma tumor syndrome spectrum has broadened to include Proteus syndrome and Proteus-like syndromes. Exon 5, which encodes the core motif, is a hotspot for mutations likely due to the biology of the protein. PTEN is a major lipid 3-phosphatase, which signals down the PI3 kinase/AKT pro-apoptotic pathway. Furthermore, PTEN is a protein phosphatase, with the ability to dephosphorylate both serine and threonine residues. The protein-phosphatase activity has also been shown to regulate various cell-survival pathways, such as the mitogen-activated kinase (MAPK) pathway. Although it is well established that PTEN's lipid-phosphatase activity, via the PI3K/AKT pathway, mediates growth suppression, there is accumulating evidence that the protein-phosphatase/MAPK pathway is equally important in the mediation of growth arrest and other crucial cellular functions.|Animals[MESH]|Disease Models, Animal[MESH]|Germ-Line Mutation/genetics[MESH]|Hamartoma Syndrome, Multiple/genetics/metabolism[MESH]|Humans[MESH]|Mice[MESH]|PTEN Phosphohydrolase[MESH]|Phosphatidylinositol 3-Kinases/metabolism[MESH]|Phosphoric Monoester Hydrolases/*chemistry/genetics/*metabolism[MESH]|Proteus Syndrome/*genetics/metabolism[MESH]|Signal Transduction[MESH]|Structure-Activity Relationship[MESH]|Tumor Suppressor Proteins/*chemistry/genetics/*metabolism[MESH] |
