LKB1 induces apical trafficking of Silnoon, a monocarboxylate transporter, in Drosophila melanogaster.

LKB1 induces apical trafficking of Silnoon, a monocarboxylate transporter, in Drosophila melanogaster.
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DOI:
10.1083/jcb.200807052
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发表时间:
2008-10-06
期刊:
The Journal of cell biology
影响因子:
--
通讯作者:
Chung J
Chung J
中科院分区:
其他
文献类型:
--
作者:
Jang C;Lee G;Chung J

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Silnoon(Sln)是一种单羧酸转运蛋白(MCT),介导代谢性单羧酸盐(如丁酸盐和乳酸盐)的主动转运。在这里,我们确定Sln作为一种新的LKB 1相互作用的蛋白质使用果蝇遗传修饰剂筛选。Sln表达不影响细胞周期进程或细胞大小,但特异性增强LKB 1依赖性凋亡和组织大小减小。相反,Sln的下调抑制LKB1依赖的细胞凋亡,暗示Sln作为LKB1的下游介质。LKB1的激酶活性诱导极化细胞中Sln的顶端运输,并且LKB1依赖的Sln运输对于触发细胞外丁酸盐诱导的细胞凋亡至关重要。鉴于LKB1的功能是控制上皮极性和细胞死亡,我们建议Sln是LKB1的重要下游靶点。
Silnoon (Sln) is a monocarboxylate transporter (MCT) that mediates active transport of metabolic monocarboxylates such as butyrate and lactate. Here, we identify Sln as a novel LKB1-interacting protein using Drosophila melanogaster genetic modifier screening. Sln expression does not affect cell cycle progression or cell size but specifically enhances LKB1-dependent apoptosis and tissue size reduction. Conversely, down-regulation of Sln suppresses LKB1-dependent apoptosis, implicating Sln as a downstream mediator of LKB1. The kinase activity of LKB1 induces apical trafficking of Sln in polarized cells, and LKB1-dependent Sln trafficking is crucial for triggering apoptosis induced by extracellular butyrate. Given that LKB1 functions to control both epithelial polarity and cell death, we propose Sln is an important downstream target of LKB1.
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