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Development and Application of a Comprehensive Isotope-labeled Peptide Library to Quantify the Twelve Signal Transduction Pathways of Carcinogenesis

机译:综合同位素标记的肽库的开发和应用,以量化致癌生殖的十二个信号转导途径

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Development of a SIS library for twelve pathways involved in cancer using 100 proteins Quantitation of 93 proteins across twelve key pathways. Significant changes were seen in the TNF-α/NFκB induced apoptosis pathway (Figure 3 and Table 2) as has been noted previously. (1) Taxol induced expression of TNF-α, promoting TNFR2 receptor that increasing activation of NFκB and AKT1 while inhibiting phosphorylation of BAD, promoting cell proliferation and suppressing apoptosis. Significant decreases were detected for ATR and ATM (Figure 3 and Table 2), both key players in double strand break DNA repair and both the G_1 and G_2 checkpoints. (1) Inhibition of both ATM and ATR has been used to re-sensitized cisplatin resistant cells (2) Further studies are ongoing to investigate the role of these proteins in both taxol-and cisplatin-resistance.
机译:使用跨越123个蛋白质的癌症涉及癌症的12个途径的SIS文库的研制。如前所述,在TNF-α/NFκB诱导的凋亡途径(图3和表2)中看到了显着的变化。 (1)紫杉醇诱导TNF-α的表达,促进TNFR2受体,即抑制不良,促进细胞增殖和抑制细胞凋亡的磷酸化同时增加NFκB和AKT1的活化。针对ATR和ATM(图3和表2)检测到显着的降低(图3和表2),双链中的关键球员分解DNA修复和G_1和G_2检查点。 (1)对ATM和ATR的抑制已被用于重新敏化的顺铂抗性细胞(2)正在进行的进一步研究,以研究这些蛋白质在紫杉醇和顺铂抗性中的作用。

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