We found that Ku70, a known DNA repair factor, has a novel function to bind and inhibit Bax (Bcl-2-associated X protein), a key mediator of apoptosis. Pentapeptides derived from the Bax-binding domain of Ku70 were cell-permeable and protected cells from Bax-mediated apoptosis. These pentapeptides were called BIPs (Bax-inhibiting peptides). BIPs may become a useful therapeutic tool to reduce cellular damage. We also generated BIP mutant pentapeptides that do not inhibit Bax, but retain their cell-penetrating activity. Since both BIPs and BIP mutants are cell-permeable, these peptides were designated CPP5s (cell-penetrating pentapeptides). Among the CPP5s discovered, VPTLK (BIP) and KLPVM (BIP mutant) were confirmed to possess protein transduction activity by examination of the delivery of GFP (green fluorescent protein) into cells by these peptides. The mechanism of cell penetration by CPP5s is not known. CPP5s enter the cell at 0 and 4 degrees C. In preliminary studies, various inhibitors of endocytosis and pinocytosis did not show any significant suppression of CPP5 cell entry. CPP5s have very low toxicity in vitro and in vivo and so may be useful tools in order to develop non-toxic drug-delivery technologies.

译文

:我们发现,已知的DNA修复因子Ku70具有结合和抑制Bax(Bcl-2相关X蛋白)的新功能,Bax是凋亡的关键介体。源自Ku70的Bax结合结构域的五肽具有细胞渗透性,并能保护细胞免受Bax介导的细胞凋亡。这些五肽称为BIP(Bax抑制肽)。 BIPs可能成为减少细胞损伤的有用治疗工具。我们还生成了BIP突变型五肽,其不抑制Bax,但保留其穿透细胞的活性。由于BIP和BIP突变体都是细胞可渗透的,因此这些肽被称为CPP5(可穿透细胞的五肽)。在发现的CPP5中,通过检查这些肽将GFP(绿色荧光蛋白)传递到细胞中,证实VPTLK(BIP)和KLPVM(BIP突变体)具有蛋白转导活性。 CPP5s渗透细胞的机制尚不清楚。 CPP5在0和4摄氏度进入细胞。在初步研究中,内吞和胞饮作用的各种抑制剂并未显示出对CPP5细胞进入的任何明显抑制作用。 CPP5在体外和体内的毒性都非常低,因此可能是开发无毒药物递送技术的有用工具。

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