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Truncation of a 20-mer Wild Type Bim BH3 Bomain Peptide: Ideatification of the Minimum Sequence Necessary for Promoting Cell Death of Prostate Cancer (PC3) Cells

机译:截断20-MEL野生型BIM BH3 BOMAIN肽:识别促进前列腺癌(PC3)细胞的细胞死亡所需的最小序列

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Cancer cells become resistant to mitochondrial-driven apoptosis, through the up-regulation of anti-apoptotic Bcl-2 family proteins. Based on a published study showing the functional activation of the pro-apoptotic Bcl-2 protein Bax by Bim BH3 20-mer peptides [1], we have carried out systematic truncation studies on the 20-mer wild-type sequence to identify the minimal domain that can cause Bax activation and promote apoptosis in PC3 prostate cancer cells.
机译:通过抗凋亡Bcl-2家族蛋白的上调,癌细胞对线粒体驱动的细胞凋亡产生抗性。基于发表的研究,显示BIM BH3 20-MEL肽的促凋亡Bcl-2蛋白Bax的功能活化[1],我们对20-MEL野生型序列进行了系统截断研究以识别最小值可以导致BAX活化和促进PC3前列腺癌细胞中凋亡的结构域。

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