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. 2022 Jan 31;29(1):440–453. doi: 10.1080/10717544.2022.2030428

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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-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 1. — Characterization of circDIDO1 in LX2 cells. (A) The Schematic illustration showing the production of circDIDO1 from its host gene, and the validation by Sanger sequencing. (B) The existence of circDIDO1 was validated using divergent and convergent primers from cDNA or genomic DNA (gDNA) of LX2 cells. (C) Random hexamer or Oligo(dT)18 primers were used in the reverse transcription experiments, and the products were examined in by qRT-PCR. (D) The relative RNA levels of circDIDO1 and GAPDH were determined by qRT-PCR after actinomycin D treatment at the indicated times. (E) The expression of circDIDO1 and GAPDH mRNA was examined in LX2 cells treated with or without RNase R. (F) Subcellular fractionation assay indicating the distribution of circDIDO1 in the cytoplasmic and nuclear fractions of LX2 cells. *p < .05, **p < .01, and ***p < .001.