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Example sentences for: pten
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Fifty-three of 55 single sections from Pten +/+ glands that were free of a palpable mass did not show any lesions more advanced than ductal hyperplasia.
While it took one year for the entire cohort (15) of Wnt-1 TG females with a wild type Pten background to develop tumors, all Wnt-1 TG, Pten +/- females showed tumors by 5 months of age.
The gene product of PTEN ( phosphatase and tensin homolog deleted from chromosome 10) is a lipid phosphatase that reverses the activities of phosphatidylinositol 3-kinase (PI3K) by dephosphorylating the D3 position of its lipid products, phosphatidylinositol-3, 4 bis-phosphate (PtdIns(3,4)P2), phosphatidylinositol-3,5 bis-phosphate (PtdIns(3,5)P2), and 3,4,5-tri-phosphate (PtdIns(3,4,5)P3) [ 2, 3], the elevated levels of which are linked to the transforming ability of PI3K [reviewed in ref.
LOH at the Pten locus has recently been reported in mammary tumors arising in Pten heterozygous mice [ 26], but only 4% of the mice developed tumors before the age of 30 weeks, and, in our cross, none of the Pten +/- mice without the Wnt-1 transgene had a palpable mammary tumor before the age of 30 weeks.
The cell surface expressed integrins can control this process by physically interacting with the extracellular matrix proteins and other cell surface proteins on endothelial cells lining the blood vessel wall [ 1 ] . These integrins signal adhesion and migration by communicating with several tyrosine kinases inside the cell, including the Focal Adhesion Kinase (FAK) and Src family kinases [ 1 2 ] . Src kinases control the activation of FAK, as well as the tyrosine phosphorylation of critical substrates that regulate adhesion and migration [ 3 ] . Indeed, colon cancer cells with high metastatic potential have elevated levels of Src activity or activating mutations in the Src gene [ 4 5 ] . One Src substrate that is involved in regulating an important signaling node in this process is the adaptor protein p130 cas (Cas) [ 6 7 8 9 10 ] . Cas appears to play a central role in the transformation process by several oncogenes including ras, ornithine decarboxylase (ODC), v-Src, v-crk, and Bcr-Abl, as these tumors all have elevated levels of tyrosine phosphorylated Cas [ 6 11 12 13 ] . Cells from mice that lack Cas have much reduced migration and are resistant to transformation by v-Src, while expression of Cas anti-sense RNA in cells transformed with ras, v-Src or ODC result in reversion of the transformed phenotype [ 11 14 15 ] . Furthermore, increased expression of Cas can rescue cell migration and adhesion in cells expressing the tumor suppressor PTEN, and can enhance cell migration and adhesion in normal cells, with a major role being played by the substrate domain [ 16 17 ] .
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