Thomas and colleagues (pp. 1122-1133) demonstrate severe dysregulation of developmentally regulated alternative splicing and polyadenylation in congenital myotonic dystrophy (CDM). In doing so, they also highlight the importance of these post-transcriptional processes during normal fetal muscle development. Finally, they generate and characterize a mouse model of CDM that lacks all three Muscleblind-like proteins.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5538429 | PMC |
http://dx.doi.org/10.1101/gad.302893.117 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!