Mirko Völkers

The paper examines the relationship between the ER and SR in cardiac myocytes, finding that the SR becomes the primary site of protein synthesis in adult cells, while the ER retains specialized functions.

This study identifies MLP as a non-canonical RNA-binding protein in cardiomyocytes and shows its RNA-dependent interaction with cytoskeletal complexes.

This study shows that loss of eEF1A2 in cardiomyocytes causes cardiomyopathy through proteostasis defects, and mTORC1 inhibition can reverse the condition.

The paper identifies NMD targets and activity in cardiomyocytes using SMG1 inhibition and RNA sequencing, showing conserved targets and reduced efficiency with UPF1/UPF2 knockdown.

This study investigates ZEB1's role in cardiomyocyte structure and function, finding that its deletion causes sarcomere damage, mitochondrial dysfunction, and dedifferentiation, particularly in females.

The paper curates a cross-species multimodal database of gene expression in cardiac hypertrophy and introduces an interactive web tool for exploring gene expression across multiple omics layers.

This study shows that Ythdf2, an m6A reader protein, regulates cardiac function by controlling gene expression through its target transcripts, leading to cardiac remodeling in heart failure models.

This study investigates the role of RPL3L in ribosome heterogeneity and mitochondrial activity in cardiomyocytes, finding that its depletion increases ribosome-mitochondria interactions and ATP levels.

This study shows that temporarily inhibiting protein translation after heart attack reduces inflammation and improves long-term heart function by targeting the mTORC1-4EBP1-eIF4F pathway.

This study shows that the unfolded protein response declines with age in the heart, leading to protein misfolding and cardiac dysfunction.

The paper identifies Cand2 as an mTORC1-regulated gene that promotes adverse cardiac remodeling when overexpressed, and shows its deletion protects the myocardium.

The paper compares transcriptome and translatome networks in cardiac remodeling to identify differences in gene regulation and functional modules.