Analysis of cardiac gene expression in juvenile versus mature mice with repressed CELF activity (MHC-CELFdelta)

ABSTRACT: CUG-BP, Elav-like family (CELF) proteins regulate alternative splicing. In MHC-CELFdelta transgenic mice, CELF-mediated alternative splicing is disrupted in heart muscle via expression of a nuclear dominant negative CELF protein under an alpha-myosin heavy chain promoter. MHC-CELFdelta mice develop dilated cardiomyopathy and contractile dysfunction by 3 weeks of age, shortly after the transgene is activated and splicing defects appear. Cardiac function and heart size spontaneously recover with age in a low-expressing (mild) line of MHC-CELFdelta mice despite persistence of dominant negative protein expression and splicing defects, whereas there is no recovery in a higher-expressing (severe) line that also experiences early muscle death and fibrosis. In this study, we explored the basis

ORGANISM(S): Mus musculus

SUBMITTER: John Barnard 

PROVIDER: E-GEOD-62363 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress