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. 2021 Mar;81:100883. doi: 10.1016/j.preteyeres.2020.100883

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© 2020 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Fig. 3 — Mechanisms of cellular dysregulation associated with CTG18.1 expansions. Four non-mutually exclusive mechanisms have been proposed to drive and/or exacerbate the onset of CTG18.1 expansion-mediated FECD, including; (1) dysregulated expression of TCF4 transcripts, (2) accumulation of toxic (a) sense (CUG)_n and (b) antisense-derived (CAG)_n repetitive RNA transcripts, (3) RAN translation of repetitive RNA transcripts, and (4) age and tissue-dependant somatic instability of the repeat element.