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GD3-7-醛是一种凋亡诱导剂,可与腺嘌呤核苷酸移位酶相互作用。

GD3-7-aldehyde is an apoptosis inducer and interacts with adenine nucleotide translocase.

机构信息

University of Versailles-SQY, PRES UniverSud Paris, CNRS UMR8159, 45 Avenue des Etats-Unis, 78035 Versailles, France.

出版信息

Biochem Biophys Res Commun. 2010 Jan 1;391(1):248-53. doi: 10.1016/j.bbrc.2009.11.044. Epub 2009 Nov 11.

Abstract

We prepared GD3-7-aldehyde (GD3-7) and determined its apoptotic potential. GD3-7 proved to be more efficient to induce pro-apoptotic mitochondrial alterations than GD3 when tested on mouse liver mitochondria. GD3-7-induced mitochondrial swelling and depolarization was blocked by cyclosporin A (CsA) supporting a critical role of the permeability transition pore complex (PTPC) during GD3-7-mediated apoptosis. In contrast to GD3, GD3-7 was able to induce channel formation in proteoliposomes containing adenine nucleotide translocase (ANT). This suggests that ANT is the molecular target of GD3-7. Using a specific antiserum, GD3-7 was detected in the lipid extract of the myeloid tumor cell line HL-60 after apoptosis induction, but not in living cells. Therefore, GD3-7 might be a novel mediator of PTPC-dependent apoptosis in cancer cells.

摘要

我们制备了 GD3-7-醛(GD3-7),并确定了其凋亡潜能。当在小鼠肝线粒体上进行测试时,GD3-7 被证明比 GD3 更有效地诱导促凋亡的线粒体改变。GD3-7 诱导的线粒体肿胀和去极化被环孢素 A(CsA)阻断,这支持了在 GD3-7 介导的细胞凋亡过程中通透性转换孔复合体(PTPC)的关键作用。与 GD3 相反,GD3-7 能够在含有腺嘌呤核苷酸转运蛋白(ANT)的脂蛋白体中诱导通道形成。这表明 ANT 是 GD3-7 的分子靶标。使用特异性抗血清,在诱导凋亡后,髓样肿瘤细胞系 HL-60 的脂质提取物中检测到 GD3-7,但在活细胞中未检测到。因此,GD3-7 可能是癌细胞中 PTPC 依赖性细胞凋亡的新型介质。

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