MicroRNA expression data from a heterozygous Titin-deficient mouse model and wildtype controls

ABSTRACT: Mutations in the sarcomeric protein titin are a major cause of human dilated cardiomyopathy. We have developed a knock-in mouse model that imitated a previously identified titin truncation mutation. The heterotygous Ttn-deficient mice develop features of DCM and therefore recapitulate the human phenotype. To investigate the role of microRNAs in titin-based heart failure, we performed a miRNA screen in heterozygous Ttn-deficient mice and their wildtype littermate controls.

ORGANISM(S): synthetic construct Mus musculus

PROVIDER: GSE90972 | GEO | 2017/01/31

SECONDARY ACCESSION(S): PRJNA356509

REPOSITORIES: GEO