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自噬调节唾液酸转运蛋白(一种溶酶体唾液酸转运体)的稳定性。

Autophagy regulates the stability of sialin, a lysosomal sialic acid transporter.

作者信息

Huang Chengcheng, Seino Junichi, Wang Li, Haga Yoshimi, Suzuki Tadashi

机构信息

a Glycometabolome Team, Systems Glycobiology Research Group, RIKEN-Max Planck Joint Research Center for Systems Chemical Biology , RIKEN Global Research Cluster , Wako , Japan.

出版信息

Biosci Biotechnol Biochem. 2015;79(4):553-7. doi: 10.1080/09168451.2014.991682. Epub 2014 Dec 15.

Abstract

Macroautophagy plays a critical role in catabolizing cytosolic components via lysosomal degradation. Recent findings from our studies indicate that basal autophagy is required for the efficient lysosomal catabolism of sialyloligosaccharides, and that the downregulation of sialin, a lysosomal transporter of sialic acids can cause a significant delay in the cytosolic accumulation of such glycans. The findings reported herein show that the sialin protein level was increased when the autophagy process was inhibited. This effect appears to be specific to sialin, since the amount of LAMP1, another lysosomal membrane protein, remains constant under the same conditions. Our results suggest that autophagy may regulate the stability of sialin, and it could lead to the cytosolic accumulation of sialyloligosaccharides in autophagy-defective cells.

摘要

巨自噬在通过溶酶体降解分解胞质成分中起关键作用。我们研究的最新发现表明,基础自噬是唾液酸寡糖有效溶酶体分解代谢所必需的,并且唾液酸的溶酶体转运蛋白——唾液酸转运蛋白的下调会导致此类聚糖在胞质中的积累显著延迟。本文报道的研究结果表明,当自噬过程受到抑制时,唾液酸转运蛋白的水平会升高。这种效应似乎是唾液酸转运蛋白特有的,因为在相同条件下,另一种溶酶体膜蛋白LAMP1的量保持不变。我们的结果表明,自噬可能调节唾液酸转运蛋白的稳定性,并且这可能导致自噬缺陷细胞中唾液酸寡糖在胞质中的积累。

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