Philipp F. Lange

This study uses single-cell proteomics to identify patient-specific subpopulations in pediatric B-ALL, revealing relapse-prone phenotypes and potential for personalized therapy.

ProteoForge identifies differential proteoforms by imputing missing data in bottom-up proteomics, showing high accuracy in complex datasets and revealing hidden proteoform regulation in lung cancer cells under hypoxia.

This study uses hiPSC-derived cardiomyocytes to model CRDS, showing that programmed electrical stimulation induces arrhythmias through EADs and re-entry, which can be suppressed by flecainide.

This study investigates how metabolic maturation affects molecular and metabolic states in hiPSC-derived cardiomyocytes with TNNT2-linked hypertrophic cardiomyopathy, revealing variant-specific disruptions in metabolic pathways and gene regulation.

This study shows that passaging hiPSC-derived cardiac fibroblasts activates them to myofibroblasts, involving TGFβ1, Hippo signaling, and mitochondrial metabolism changes.

This paper develops a micropatterned substrate to enhance maturation of hiPSC-CMs, finding optimal maturation occurs at three weeks on a soft PDMS substrate.

The paper analyzes protein levels and solubility in brain regions of aged mice, revealing age-related changes in proteostasis and inflammation markers.

The paper shows that TBP is not essential for Pol II transcription in mESCs, revealing a TBP-independent mechanism for transcription initiation.

The paper introduces RoLiM, an algorithm for detecting protease activities in peptide data, identifying known and novel cleavage patterns in cancer and viral contexts.

This study uses multi-omic profiling of blood samples from ALD patients to identify molecular markers predictive of cerebral demyelination, but finds no statistically significant markers due to high inter-individual variation.