SRp38 Regulates Alternative Splicing and Is Required for Ca2+ Handling in the Embryonic Heart
Open Access
- 1 April 2009
- journal article
- research article
- Published by Elsevier in Developmental Cell
- Vol. 16 (4), 528-538
- https://doi.org/10.1016/j.devcel.2009.02.009
Abstract
No abstract availableKeywords
Funding Information
- National Institutes of Health (GM48259)
This publication has 43 references indexed in Scilit:
- Phosphorylation switches the general splicing repressor SRp38 to a sequence-specific activatorNature Structural & Molecular Biology, 2008
- Splicing in disease: disruption of the splicing code and the decoding machineryNature Reviews Genetics, 2007
- An intronic element contributes to splicing repression in spinal muscular atrophyProceedings of the National Academy of Sciences, 2007
- Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardiaJournal of Clinical Investigation, 2006
- Inactivation of the SR Protein Splicing Factor ASF/SF2 Results in Genomic InstabilityCell, 2005
- Triadin Overexpression Stimulates Excitation-Contraction Coupling and Increases Predisposition to Cellular Arrhythmia in Cardiac MyocytesCirculation Research, 2005
- ASF/SF2-Regulated CaMKIIδ Alternative Splicing Temporally Reprograms Excitation-Contraction Coupling in Cardiac MuscleCell, 2005
- Involvement of SR Proteins in mRNA SurveillanceMolecular Cell, 2004
- Dephosphorylated SRp38 acts as a splicing repressor in response to heat shockNature, 2004
- Cardiac Hypertrophy and Impaired Relaxation in Transgenic Mice Overexpressing Triadin 1Journal of Biological Chemistry, 2001