L line BCM1, the expression of both genes is opposite: no levels of MAGE-A1 [2^(Ct) 1.07] and high levelsof BORIS [2^(Ct) 24.39]. We transiently transfected expression plasmid encoding BORIS into both cell lines, with negligible transcript levels of MAGE-A1, and quantified endogenous MAGE-A1 mRNA by RT (reverse transcription)-PCR and gel electrophoresis. As depicted in Figure 1, BORIS was able to

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To mediate ADCC in vitro [9, 17, 23]. Although the contribution of ADCC activity to clinical efficacy is unclear, it is important to characterize all activities of the candidate mAb, especially those that can be affected by differences in post-translational modifications, such as glycosylation. The ability of ABP 501 to induce ADCC was assessed using MT-3 cells as target cells, and NK-92M1 cells s

To mediate ADCC in vitro [9, 17, 23]. Although the contribution of ADCC activity to clinical efficacy is unclear, it is important to characterize all activities of the candidate mAb, especially those that can be affected by differences in post-translational modifications, such as glycosylation. The ability of ABP 501 to induce ADCC was assessed using MT-3 cells as target cells, and NK-92M1 cells s

To mediate ADCC in vitro [9, 17, 23]. Although the contribution of ADCC activity to clinical efficacy is unclear, it is important to characterize all activities of the candidate mAb, especially those that can be affected by differences in post-translational modifications, such as glycosylation. The ability of ABP 501 to induce ADCC was assessed using MT-3 cells as target cells, and NK-92M1 cells s

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