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首页> 外文期刊>Journal of cellular physiology. >LncRNA NEAT1 induces autophagy through epigenetic regulation of autophagy-related gene expression in neuroglial cells
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LncRNA NEAT1 induces autophagy through epigenetic regulation of autophagy-related gene expression in neuroglial cells

机译:通过表观遗传LncRNA NEAT1诱发自噬autophagy-related调节基因的表达神经胶质细胞

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摘要

Endocytosis and autophagy are two important pathways for amyloid-β (Aβ) clearance in neuroglial cells. Our previous study demonstrated that nuclear paraspeckle assembly transcript 1 (NEAT1) long noncoding RNA modulates Aβ clearance mediated by neuroglial cells via the epigenetic regulation of endocytosis-related genes. Herein, we demonstrate that NEAT1 functions as an autophagy inducer by modulating the expression of multiple autophagy-related genes, including autophagy-related 5 (atg5), autophagy-related 3 (atg3), and beclin1. NEAT1 can promote transcription of these genes by altering histone modification near these transcrip-tional start sites of the genes and thereby influencing the recruitment of signal transducer and activator of transcription 3 to these gene promoters. Our findings demonstrate a new cellular function of NEAT1 in neuroglial cells and suggest a potential therapeutic target for the treatment of autophagy-related diseases.
机译:内吞作用和自噬是两个重要的途径-β淀粉样蛋白(β)间隙神经胶质细胞。核paraspeckle大会记录1(NEAT1)长非编码RNA调节β间隙通过表观遗传由神经胶质细胞endocytosis-related基因的调控。我们作为一个证明NEAT1功能自噬诱导物调制的表达多个autophagy-related基因,包括autophagy-related 5 (atg5), autophagy-related 3(atg3)和beclin1。这些基因通过改变组蛋白的转录修改这些transcrip-tional开始附近网站的基因,从而影响招聘的信号传感器和催化剂这些基因启动子转录3。调查结果表明新细胞的功能NEAT1神经胶质细胞和显示一个潜在的治疗的治疗目标autophagy-related疾病。

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