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Or his help with radial migration assays. Reagents used in preliminary pilot assays were kindly provided by Yoel Kloog Authors' contributions LGT and JHU conceived of the study and designed the assays. LGT performed tumor xenografting, cell culture, and laser capture microdissection. LGT, FL, and RK wrote and edited the manuscript. AN designed and performed all DNA vector construction and sequenci
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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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Man T lymphocytes. J Immunol 1998, 161:2114?119. 47. Rubinstein N, Alvarez M, Zwirner NW, Toscano MA, Ilarregui JM, Bravo A, Mordoh J, Fainboim L, Podhajcer OL, Rabinovich GA: Targeted inhibition of galectin-1 gene expression in tumor cells results in heightened T cellmediated rejection; A potential mechanism of tumor-immune privilege. Cancer Cell 2004, 5:241?51. 48. Kuppner MC, Hamou MF, Sawamura
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Man T lymphocytes. J Immunol 1998, 161:2114?119. 47. Rubinstein N, Alvarez M, Zwirner NW, Toscano MA, Ilarregui JM, Bravo A, Mordoh J, Fainboim L, Podhajcer OL, Rabinovich GA: Targeted inhibition of galectin-1 gene expression in tumor cells results in heightened T cellmediated rejection; A potential mechanism of tumor-immune privilege. Cancer Cell 2004, 5:241?51. 48. Kuppner MC, Hamou MF, Sawamura
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Assays of GBM cells stably transfected to over-express galectin-1, perfectly fit in with the previous studies mentioned above and highlight the importance of galectin-1 in the biologically aggressive behavior of experimental GBMs. While there was no enhancement of proliferation or change inattachment to fibronectin, galectin-1 upregulation induced more rapid two-dimensional migration and enhanced
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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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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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With a narrow tip, the yolk cell can be disrupted. A buffer of low osmolarity facilitated the dissolving of the yolk. The deyolking efficiency was further increased by two additional wash steps. By removing the yolk proteins this method efficiently decreased the total protein amount per embryo more than 10 fold from 55 to 3 per embryo (Fig. 2A and 2B). However, recovery of cellular proteins rema