Mutations in the tissue-specific ribosomal protein RPL3L lead to infant dilated cardiomyopathy. The current project aims to understand the mechanistic details of disease progression using in vivo biopsies from transplanted heart of patient with RPL3L mutations as well as engineered AC16 cell lines that express the same and other RPL3L variants containing a C-terminal HA tag. The files consist of two datasets from human left ventricle (LV) and human AC16 cells, respectively. The human LV samples are two technical replicates from the same biopsy. The AC16 cell samples are immunoprecipitations of HA-tagged RPL3L in nuclear extracts.