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Is transcriptionaly regulated by ERK in response to Triphala treatment suggesting ERK as an upstream regulator of p53 in Capan-2 cells. We also observed that Triphala induce apoptosis by ERK activation in BxPC-3 cells, which has mutated p53. This is in part consistent with the observation that activated ERK lead to apoptosis after DNA damage in a p53 independent manner [49]. On the other hand, Tri
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Nd on the abundance of the target protein. If the yolk is not removed manually, then only 1 or 2 embryos (50?00 ) can be loaded per lane on a gel to avoid overloading effects due to yolk protein. This limits the sensitivity for cellular proteins. The deyolking method enabled us to load significantly more embryos and therefore the signal from specific cellular proteins was increased.Figure 3 demon
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Bryos In the early embryo, the cells forming the embryo proper constitute only a minor volume of the embryo compared to the large yolk cell (Fig. 1B). The abundance of yolk proteins interferes with any proteomic application that intends to target the cells of the embryo proper. The major yolk protein Vitellogenin, a phospholipo-glycoprotein,Page 1 of(page number not for citation purposes)BMC Devel
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Ing glioblastoma cells to apoptosis. J Clin Oncol 2005, 23: 2411?422. Paulus W, Baur I, Beutler AS, Reeves SA: Diffuse brain invasion of glioma cells requires beta 1 integrins. Lab Invest 1996, 75:819?26. Uhm JH, Gladson CL, Rao JS: The role of integrins in the malignant phenotype of gliomas. Front Biosci 1999, 4:D188 199. Lipinski CA, Tran NL, Bay C, Kloss J, McDonough WS, Beaudry C, Berens ME, L
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Ble cross-hybridizing host genes. The use of our animal model to identify mediators of glioma invasion has the potential pitfall of identifying artifacts of xenografting. That is, human glioma cells confronted with nude mouse brain rather than human brain may express genes specific to this setting. Two arguments can be made against this theory. First, there is no teleological reason for human cell