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Phosphatase and tensin homology

All phosphoinositides are found in the cytosolic half of the lipid bilayer of the plasma or intracellular compartment membranes (left part). The different kinases acting on phosphoinositides in mammalian cells are shown in solid lines and the phosphoinositide 3-kinases, in bold. The phosphoinositides counterpart pathways catalysed by known phosphatases are represented by dashed lines. The best known phosphatases are PTEN (Phosphatase and tensin homolog deleted on chromosome 10) and SHIP (SH2 domain-containing inositol 5-phosphatase). [Pg.971]

Phospholipid phosphatases are enzymes such as SHIP (SH2-domain containing inositide-5-phosphatase) or PTEN (phosphatase and tensin homolog deleted on chromosome 10) which dephosphorylate phosphoino-sitides. Whereas SHIP removes phosphate from the 5 ... [Pg.975]

PBD peroxisome biogenesis disorders PTEN phosphatase and tensin homolog... [Pg.966]

Seo JH, Ahn Y, Lee SR, Yeol YC, Chung HK. 2005. The major target of the endogenously generated reactive oxygen species in response to insulin stimulation is phosphatase and tensin homolog and not phosphoinositide-3 kinase (PI-3 kinase) in the PI-3 kinase/Akt pathway. Mol Biol Cell 16 348-357. [Pg.227]

PTEN, phosphatase and tensin homolog PTPase, phosphotyrosine phosphatase PYY, peptide YY... [Pg.1027]

Inactivation of these signaling pathways is mediated by phosphoinositide-specilic phosphatases such as phosphatase and tensin homolog (PTEN). PTEN is a tumor suppressor protein that is mutated in several human cancers. Loss of PTEN results in unregulated cell survival, and thus aberrant cell growth. [Pg.111]

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. [Pg.564]

LAST2 - large tumor suppressor 2 PTEN - phosphatase and tensin homolog TPMl - tumor-suppressor tropomyosin-1. [Pg.456]

The loss of function deletion/mutation in the phosphatase and tensin homolog (PTEN) tumor-suppressor loeus is found to occur in 30 0% of GBM patients [16, 17]. PTEN is a regulator of the pro-growth kinases, PI3K and AKT. Phosphorylation of these proteins can activate pro-growth/pro-survival... [Pg.479]

Table VIII Phosphatase and Tensin Homolog on Chromosome Ten (PTEN)... Table VIII Phosphatase and Tensin Homolog on Chromosome Ten (PTEN)...
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 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.

See other pages where Phosphatase and tensin homology is mentioned: [Pg.55]    [Pg.466]    [Pg.58]    [Pg.248]    [Pg.349]    [Pg.605]    [Pg.81]    [Pg.50]    [Pg.52]    [Pg.207]    [Pg.394]    [Pg.404]    [Pg.249]    [Pg.311]    [Pg.289]    [Pg.19]    [Pg.1646]    [Pg.344]    [Pg.468]    [Pg.131]    [Pg.508]    [Pg.131]    [Pg.281]    [Pg.197]    [Pg.429]    [Pg.384]    [Pg.29]    [Pg.318]    [Pg.299]    [Pg.99]   


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