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. 2022 Jan 11;13(1):1858–1871. doi: 10.1080/21655979.2021.2018386

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© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — METTL14 overexpression repressed ASS1 mRNA stability via an m6A-YTHDF2-dependent pathway. A. YTHDF2 expression in GBM tissues and normal tissues were analyzed by GEPIA database (http://gepia.cancer-pku.cn/). B. Transfected U87 and U251 cells with YTHDF2 overexpression plasmid or shRNA, and the interference efficiency was detected by qRT-PCR. C. The mRNA levels of YTHDF2 and ASS1 in YTHDF2 overexpression or knockdown glioma cells were detected by qRT-PCR. D. The protein levels of YTHDF2 and ASS1 in YTHDF2 overexpression or knockdown glioma cells were detected by Western blot. E. Precursor and mature mRNA of ASS1 in METTL14 overexpression or knockdown and control glioma cells. F-G. The precursor (f) and mature (g) ASS1 mRNA expression were detected at indicated times. H. RIP-qPCR assay using YTHDF2-specifc antibody and IgG control antibody to measure the enrichment of YTHDF2 binding to ASS1 m6A modification sites. *p < 0.05; **p < 0.01; ***p < 0.001.