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Ns.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 2 ofgrowth factor receptors [11] to effector metallo- [12,13] and serine- [14] proteases. Galectin-1 has also been identified as a key player in GBM cell mi
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Ca, MA) and rested for 24 hours. 0.1 and 1 M of TAK733 or parallel DMSO vehicle control were added in triplicate for 20 hours. Cells were incubated for 1 hour with 2.0 Ci with metabolic tracers chosen as analogues of PET tracers: 3H-DDG (American Radiolabeled Chemicals Inc., St. Louis, MO) in glucose-free RPMI 1640 (Invitrogen), or methyl-3H-thymidine (thymidine, Moravek Biochemicals Inc., Brea, C
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Ting allows for harvesting of normal host brain from regions remote from the tumor, which serve as a control for possible contamination of samples microdissected at the tumor-brain interface. Galectin-1 was thus identified in this unsupervised method of analysis as a key marker of glioma invasion, while validating the novel filtering method (used to control for sample contamination) presented in t
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Small-sample protocol recommendations, and GeneChip hybridization followed our standard protocol [28]. After washes, arrays were scanned using the GeneChip Scanner 3000 (Affymetrix, Santa Clara, CA). Light intensity data from all spots on each chip were recorded as .cel files, stored on an internal server, and written to a digital variable disc (DVD).Data normalization and filteringreproducibility
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Id tumors. J Clin Oncol 2010, 28:611s. Hall-Jackson CA, Eyers PA, Cohen P, Goedert M, Boyle FT, Hewitt N, Plant H, Hedge P: Paradoxical activation of Raf by a novel Raf inhibitor. Chem Biol 1999, 6:559?68. Su F, Viros A, Milagre C, Trunzer K, Bollag G, Spleiss O, Reis-Filho JS, Kong X, Koya RC, Flaherty KT, et al: RAS mutations in cutaneous squamous-cell carcinomas in patients treated with BRAF in
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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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