Marieluise Kirchner

This study shows that neuroblastoma-derived sEVs retain genomic subgroup and lineage state signatures from their parental cells.

This study identifies SVIL haploinsufficiency as a cause of hypertrophic cardiomyopathy by impairing mechanotransduction and cellular energetics, with potential therapeutic implications for mitochondrial-targeted treatments.

The paper shows UBE3C regulates cortical neurogenesis and glial fate through m6A methylation, with mutations disrupting this process and offering therapeutic targets.

This study uses proteomics to compare the systemic effects of two CFTR modulator therapies in CF patients, finding that ELX/TEZ/IVA leads to proteome changes closer to healthy profiles.

The paper identifies novel E-box interactors using proximity labeling proteomics in mouse fibroblasts, revealing proteins involved in circadian transcription regulation.

The paper models BCR signaling in B cell lymphoma cells to identify conserved network structures and crosstalk mechanisms.

The paper identifies phosphorylation sites in PLPPR3 and shows that phosphorylation at S351 regulates its interaction with BASP1, suggesting a role for the PLPPR3-BASP1 complex in synaptic signaling.

This study identifies Arl8b as a potential biomarker for Alzheimer's disease by analyzing proteomic changes in 5xFAD mouse brain regions and CSF from AD patients.

The paper introduces a method to identify zipcodes in neurons, finding two new zipcodes in mouse primary cortical neurons.

This study shows that modifying the C-terminal of EAAT2 in a Huntington's disease mouse model reduces hypokinesia symptoms by improving glutamate clearance and reversing some HD-induced changes in EAAT2 interactions.