Phosphatase and tensin homology deleted on chromosome ten

Qiao, J., Kang, J., Cree, J., Evers, B. M., Chung, D. H. (2005). Gastrin-releasing peptide-induced down-regulation of tumor suppressor protein PTEN (phosphatase and tensin homolog deleted on chromosome ten) in neuroblastomas. Annals of Surgery, 241, 684-691. 

Figure 3. Pathways of phosphoinositide synthesis and interconversions. The figure shows the main pathways of phosphoinositide synthesis in mammalian cells. For the sake of clarity only the enzymatic activities (3-, 4- or 5-kinases or phosphatases) are indicated. In some cases the identification of key enzymes is mentioned (class I, II and III PI 3-kinases, PTEN, MTM, MTMR or SHIP). PI3K, phosphoinositide 3-kinase. PTEN, phosphatase and tensin homolog deleted on chromosome ten. MTM, myotubularin. MTMR, myotubular myopathy-related protein. SHIP, Src homology 2-containing inositol 5-phosphatase. PLC, phospholipase C. DAG, diacylglycerol.

Figure 50. PTEN. The tumor suppressor gene and gene product protein PTEN (phosphatase tensin homolog deleted on chromosome ten, human 10q23.3) (Table VIII), is the natural inhibitor of oncogenes PI3K/Akt (phosphatidyl inositol kinase 3 protein kinase 3 phosphatidylinositol 3 phosphate Jacob Furth s AK mouse strain thymic lymphoma retroviral oncogene phosphoinosite-dependent kinase). The PTEN protein inactivates PIP3 by dephosphorylation PDKl (phosphoinositol-dependent kinase) is not recruited to the plasma membrane to activate Akt by phosphorylation. Sarah M. Planchon et al. The nuclear affairs of PTEN. J Cell Sci 2008 121 249-253. doi 10.1242/jcs.022459...

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