Ataxin-10 interacts with O-GlcNAc transferase OGT in pancreatic β cells
Ataxin-10 interacts with O-GlcNAc transferase OGT in pancreatic β cells
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DOI：
10.1016/j.bbrc.2005.09.026
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发表时间：
2005-11-11
影响因子：
3.1
通讯作者：
Özcan, S
中科院分区：
文献类型：
--
作者：
Andrali, SS;März, P;Özcan, S
一些后生动物的细胞核和细胞质蛋白被O-linked N-acetylglucosamine （O-GlcNAc）修饰。这种修饰是动态和可逆的，类似于磷酸化，由O-linked GlcNAc转移酶（OGT）催化。高血糖已被证明会增加胰腺β细胞中的O-GlcNAc水平，这似乎会干扰β细胞的功能。为了更好地了解O-linked GlcNAc修饰在β细胞中的作用，我们从小鼠胰岛素瘤MIN6细胞系的cDNA文库中分离出OGT相互作用蛋白。我们在此描述了由SCA10（脊髓小脑共济失调10型）基因编码的Ataxin-10作为一种OGT相互作用蛋白的鉴定。SCA10基因突变导致进行性小脑共济失调和癫痫发作。我们在体内证明了SCA10与OGT相互作用，并在MIN6细胞中被o -链糖基化修饰，这表明Ataxin-10蛋白在胰腺β细胞中具有新的作用。(c) 2005爱思唯尔公司版权所有。
Several nuclear and cytoplasmic proteins in metazoans are modified by O-linked N-acetylglucosamine (O-GlcNAc). This modification is dynamic and reversible similar to phosphorylation and is catalyzed by the O-linked GlcNAc transferase (OGT), Hyperglycemia has been shown to increase O-GlcNAc levels in pancreatic beta cells, which appears to interfere with beta-cell function. To obtain a better understanding of the role of O-linked GlcNAc modification in beta cells, we have isolated OGT interacting proteins from a cDNA library made from the mouse insulinoma MIN6 cell line. We describe here the identification of Ataxin-10, encoded by the SCA10 (spinocerebellar ataxia type 10) gene as an OGT interacting protein. Mutations in the SCA10 gene cause progressive cerebellar ataxias and seizures. We demonstrate that SCA10 interacts with OGT in vivo and is modified by O-linked glycosylation in MIN6 cells, suggesting a novel role for the Ataxin-10 protein in pancreatic beta cells. (c) 2005 Elsevier Inc. All rights reserved.