Key result
Srsf5 deletion in mice resulted in perinatal lethality and cardiac dysfunction with noncompaction of the ventricular myocardium due to disrupted alternative splicing of Myom1.
Why the study?
The functional role of SRSF5 in tissue development and disease remains unknown.
Population
Srsf5 knockout (Srsf5-/-) mice generated using CRISPR-Cas9
Comparison
Srsf5-/- mice vs control mice
Design
Preclinical animal knockout study
Authors
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Srsf5 loss causes lethal murine cardiomyopathy; leaves open relevance to human noncompaction and requires validation before clinical consideration.
Srsf5 is essential for normal heart development, and its deletion causes perinatal lethality and ventricular noncompaction by disrupting alternative splicing of Myom1.
Zhang et al. (2021) studied Noncompaction of ventricular myocardium. Srsf5 deletion (CRISPR-Cas9 knockout) was evaluated on Cardiac development and function. Srsf5 deletion in mice resulted in perinatal lethality and cardiac dysfunction with noncompaction of the ventricular myocardium due to disrupted alternative splicing of Myom1.
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