2024年8月23日 · 反义寡核苷酸 (Antisense oligonucleotides, ASO) 是一种能诱导基因沉默的寡核苷酸。 一般而言，ASO的长度为15-22个核苷酸，它们被设计成与目标RNA反向互补，因此被称为反义寡核苷酸。 ASO常见的用途有三种： 可变剪接研究： 根据pre-mRNA序列设计ASO，使其与目标pre-mRNA的外显子及内含子的交界处互补。 ASO与pre-mRNA配对形成的双链区域能够遏制该位置被识别，引起与ASO互补的外显子在pre-mRNA成熟过程中被整段剪切掉。 通过这种方 …

2023年7月4日 · ASO是一种单链寡核苷酸分子（18~30nt），可以是DNA、RNA或DNA/RNA的杂合单链，进入细胞后可通过与靶序列互补，在 核糖核酸酶H1 （RNase H1)的作用下导致mRNA降解，从而抑制蛋白表达；或通过空间位阻效应实现pre-mRNA的选择性剪接，调控基因的翻译，达 …

2020年7月9日 · In this study, we utilize PMO and 2′MOE to design a therapeutic approach that could address patients with monogenic loss-of-function diseases. Our approach, termed targeted augmentation of nuclear...

ASOs are synthetic oligonucleotides or oligonucleotide analogs that can be designed to bind to protein-coding RNAs as well as noncoding RNAs. They regulate RNA function through a variety of different mechanisms, depending on the types of chemical modifications, modification sites, and binding sites by which they target RNAs.

2024年10月2日 · Antisense oligonucleotides (ASOs) are a well-established therapeutic modality based on RNA interference, but low cellular uptake, limited ability to direct ASO trafficking, and a range of intracellular barriers to successful activity compromise both gene silencing outcomes and clinical translations.

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2021年3月24日 · 新冠疫情将mRNA技术带入大众视野，而同属小核酸药物的反义寡核苷酸（antisense oligonucleotides，ASO）在mRNA火爆之前就已获得成功。 反义寡核苷酸是一种单链寡核苷酸分子，单链，通常包含15-25个核苷酸。

2017年9月9日 · We recently showed that translation can be enhanced by antisense oligonucleotides (ASOs) that target upstream open reading frames. Here we report the amount of a protein can also be selectively increased using ASOs designed to hybridize to other translation inhibitory elements in 5′ UTRs.

This article summarizes several of the common mechanisms of antisense gene modulation and more importantly, considerations to take into account when designing an antisense oligonucleotide (ASO). After decades of research, there are no hard and fast design rules; it …

The combination of in vitro hERG studies and in vivo studies in rat and monkey are consistent with no direct actions by ASOs on cardiac cell function or electrical conduction at relevant concentrations and dose levels.