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. 2021 Mar 18;11:6321. doi: 10.1038/s41598-021-85453-6

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Antisense mechanism (A) and phosphorothioate (B). (A) The use of LNA oligonucleotides as inhibitors of disease—forming proteins, or reduction of harmful RNA, is based on specific hybridization to target mRNA. This duplex recruits the cellular enzyme RNase H1 that degrade the hybridized mRNA. The LNA oligonucleotide remains intact under this process and will repeatedly trigger degradation of further target mRNA; (B) the two steric configurations Rp and Sp of the phosphorothioate linkages between the nucleobases of phosphorothioate oligonucleotides.