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. 2022 Jun 15;50(6):03000605211053703. doi: 10.1177/03000605211053703

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© The Author(s) 2022

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 3. — miR-23a is a downstream target of growth arrest specific 5 (GAS5). (a) The putative binding sequences of GAS5 and miR-23a was predicted using StarBase. (b) Luciferase reporter assays showed the luciferase activity of wild-type or mutant GAS5 in 293T cells transfected with miR-23a or negative control (NC) mimic and miR-23a. (c) RNA immunoprecipitation (RIP) assays were used to analyze the interaction between GAS5 and miR-23a. (d) qRT-PCR showed the expression levels of miR-23a in CD4⁺ T cells transfected with pcDNA3.1 or pcDNA3.1/GAS5. (e) Pearson correlation analysis showed the correlation between GAS5 and miR-23a in myasthenia gravis (MG). n = 3; **P < 0.01, ***P < 0.001.