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. 2009 Aug 31;37(19):6477–6490. doi: 10.1093/nar/gkp681

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© The Author(s) 2009. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 8. — Model of mouse Clcn1 splicing regulation by multiple factors. Cis- and trans-acting factors involved in the splicing regulation of Clcn1 exon 7A are depicted. MBNL1 represses exon 7A inclusion through a region containing the 5′ region of exon 7A as well as its flanking intronic sequence. An exonic splicing enhancer (ESE) is located at the 5′ end of exon 7A. An antisense oligonucleotide (AON) previously reported (38), as well as MBNL1, might act in part through inhibiting this ESE. The facilitation of exon 7A inclusion by CELF4 is mediated by a region located in intron 6. Expanded CUG/CCUG repeat RNA may deplete MBNL proteins, resulting in the facilitation of exon 7A inclusion.