[促进治疗性糖蛋白生物生成:干预PI3K/AKT/mTOR通路]。

IF 2 4区 生物学 Q4 CELL BIOLOGY
Mohamed Mahameed, Afnan Sulieman, Duah Alkam, B. Tirosh
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引用次数: 4

摘要

在哺乳动物细胞中产生的重组糖蛋白是临床上治疗多种疾病不可缺少的药物。它们的生物制造过程费力、耗时且昂贵。在加速这一过程和降低其成本方面的投资是继续研究的主题。PI3K/Akt/mTOR信号通路是多种生理功能的关键调控因子,如增殖、全局蛋白和脂质合成,以及许多代谢途径相互作用以增加分泌能力。在这篇综述中,我们详细介绍了以前通过遗传或药物过度激活PI3K/Akt/mTOR途径来增加糖蛋白产量的各种策略,并讨论了它们的潜力和局限性。关键词:mTORC1, CRISPR,特异性生产力,翻译
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Towards Enhancing Therapeutic Glycoprotein Bioproduction: Interventions in the PI3K/AKT/mTOR Pathway].
Recombinant glycoproteins produced in mammalian cells are clinically indispensable drugs used to treat a broad spectrum of diseases. Their bio-manufacturing process is laborious, time consuming, and expensive. Investment in expediting the process and reducing its cost is the subject of continued research. The PI3K/Akt/mTOR signaling pathway is a key regulator of diverse physiological functions such as proliferation, global protein, and lipid synthesis as well as many metabolic pathways interacting to increase secretory capabilities. In this review we detail various strategies previously employed to increase glycoprotein production yields via either genetic or pharmacological over-activation of the PI3K/Akt/mTOR pathway, and we discuss their potential and limitations.Key words: mTORC1, CRISPR, specific productivity, translation.
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来源期刊
Cell structure and function
Cell structure and function 生物-细胞生物学
CiteScore
2.50
自引率
0.00%
发文量
6
审稿时长
>12 weeks
期刊介绍: Cell Structure and Function is a fully peer-reviewed, fully Open Access journal. As the official English-language journal of the Japan Society for Cell Biology, it is published continuously online and biannually in print. Cell Structure and Function publishes important, original contributions in all areas of molecular and cell biology. The journal welcomes the submission of manuscripts on research areas such as the cell nucleus, chromosomes, and gene expression; the cytoskeleton and cell motility; cell adhesion and the extracellular matrix; cell growth, differentiation and death; signal transduction; the protein life cycle; membrane traffic; and organelles.
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