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. 2021 Oct 25;10:41. doi: 10.1186/s40035-021-00267-w

Correction to: Neurodegenerative diseases: a hotbed for splicing defects and the potential therapies

Dunhui Li 1,2,#, Craig Stewart McIntosh 1,2,#, Frank Louis Mastaglia 1,2, Steve Donald Wilton 1,2, May Thandar Aung-Htut 1,2,
PMCID: PMC8543951  PMID: 34696812

Correction to: Translational Neurodegeneration (2021) 10:16 https://doi.org/10.1186/s40035-021-00240-7

Following publication of the original article [1], the authors would like to correct a formula from “T > C” to “C > T” in two paragraphs.

  1. In the third paragraph of the section Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), the correct sentence should be:

However, the synonymous C > T substitution in SMN2 exon 7 alters an exonic splicing enhancer into an exonic splicing silencer, which predominantly leads to an unstable transcript missing exon 7.

  • 2.

    In the fourth paragraph of the section Splice-switching AOs, the correct sentence should be:

The C > T substitution in SMN2 creates an exon-splicing silencer and leads to the omission of exon 7 and an unstable SMN protein that is subject to rapid ubiquitinproteasome degradation.

In addition, the authors identified an error in Fig. 4. The correct figure is given below:

Fig. 4.

Fig. 4

Milestones of the development of antisense oligonucleotide therapeutics (excluding siRNA) from bench to bedside. Approved drugs in red are splice-switching antisense oligomers. AO: antisense oligonucleotides; FDA: US Food and Drug Administration; CMV: cytomegalovirus retinitis (in immunocompromised patients); HoFH: Homozygous familial hypercholesterolemia; DMD: Duchenne muscular dystrophy; SMA: spinal muscular atrophy; HTA: Hereditary transthyretin-mediated amyloidosis; BD: Batten disease

The original article [1] has been corrected.

Footnotes

Dunhui Li and Craig Stewart McIntosh contributed equally to this work

Reference


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