Words similar to activating
Example sentences for: activating
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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 ] .
In the case of mammalian PP5, results from lipid stimulation and binding, limited proteolysis and truncation studies taken together suggest the TPR domain and the C terminus inhibit PP5 activity in a coordinated manner and that lipid binding to the TPR domain activates the enzyme in vitro [ 18 19 20 ] . In the present study we used assay conditions for Ppt1p identical to those in which PP5 was shown to be activated by removal of the TPR or C-terminal regions [ 19 ] . Under these conditions Ppt1p is also stimulated by lipids toward 32P-MBP, and activating lipids slow TPR domain proteolysis.
Therefore DHA (22:6:n3) may require retroconversion via β-oxidation to an 18 C or 20 C LC-PUFA prior to activating PPARs [ 17 33 ] . Without the use of purified FA it is difficult to distinguish whether the DHA in our fish oil preparation was retroconverted since the fish oil also provided the retroconversion products, 20:5n3 and 22:5n3 (Table 3).
Functionally, these cells are no longer capable of activating ERK 1 or 2 in response to 10 ng/ml EGF (Figure), whereas this concentration produces a strong effect in non-pretreated cells.
Yet the agonist is fully capable of activating the full signaling pathway.
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