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Erulescens green fluorescent protein; FACS: Flow-assisted cell sorting; SDS: Sodium dodecyl sulfate; MTS: 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2(4-sulfophenyl)-2 H-tetrazolium; MTT: 3-(4,5-Dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide; CCD: Charge-coupled device. Competing interests None of the listed authors have competing interests related to the publication of this man
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Activation of ERK with induction of apoptosis by various chemopreventive and chemotherapeutic agents [39-41]. In fact, oxidants have been shown to activate ERK by taking over the growth factor receptor signaling pathways [42-46]. Moreover, ERK may get activated in response to DNA damage and can phosphorylate p53 in vitro [23,24,47-49]. We found that exposure of Capan-2 or BxPC-3 cells with apoptos
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Time intervals in a time-dependent experiment. Expression and phosphorylation of ERK (Thr-202/Tyr204) and MEK-1 (Ser-217/221) was determined by western blotting. B) The effect of Triphala on the kinase activity of ERK was determined using a kit from Cell Signaling Technology, measuring the phosphorylation of Elk-1 at Ser-383. C, D) Effect of ERK inhibitor on Triphala induced apoptosis and activati
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Esthesia. At the onset of neurological symptoms, animals were sacrificed in accordance with the Mayo Clinic IACUC. Survival curves were generated from those animals (38 of 40) developing tumors (7 of 20 acGFP-only).xenograft lines is necessary to characterize completely the in vivo phenotypic alterations that accompany overexpression of galectin-1.Our model system has identified galectin-1 as a ma
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Ental counterparts. We did not observe, however, distant invasion in U87MG tumors over-expressing galectin-1. The U87MG model is in fact weakly invasive in the brains of immunocompromized mice [33,34], while it is associated with pronounced neoangiogenesis processes [37]. Further work (e.g. viral transduction) with our patient-derivedToussaint et al. Molecular Cancer 2012, 11:32 http://www.molecul
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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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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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Activation of ERK with induction of apoptosis by various chemopreventive and chemotherapeutic agents [39-41]. In fact, oxidants have been shown to activate ERK by taking over the growth factor receptor signaling pathways [42-46]. Moreover, ERK may get activated in response to DNA damage and can phosphorylate p53 in vitro [23,24,47-49]. We found that exposure of Capan-2 or BxPC-3 cells with apoptos

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