Description
B6-Rbm20 R636Q is a point mutation knock-in mouse on the C57BL/6J background carrying the pathogenic Rbm20 R636Q mutation. The model spontaneously develops left ventricular dilation and systolic dysfunction, recapitulating the major features of human dilated cardiomyopathy. It is suitable for studies of RBM20-associated disease mechanisms and evaluation of gene and pharmacological therapies