Matthias Trost

The paper introduces a hierarchical Bayesian model to handle missing data and improve differential expression analysis in proteomics by accounting for uncertainty in missing values.

This study uses single-cell proteomics to identify protein-defined chondrocyte states and other cell populations in human osteoarthritic joints, complementing single-cell transcriptomics.

This study uses proteomic analysis to reveal reprogramming in macrophages during efferocytosis, showing an alternatively activated phenotype and secretome-driven reprogramming of naive macrophages.

The paper identifies insulin receptor ubiquitination as a regulator of collagen secretion in human skin through comparative ubiquitinomics of healthy and CYLD syndrome skin.

The paper identifies how mistargeted mitochondrial proteins are rerouted to the ER and cleared via ERAD, with MARCHF6 playing a central role in maintaining proteostasis during mitochondrial dysfunction.

This study identifies pathogenic PTCD1 variants causing mitochondrial protein aggregation and cardiomyopathy by disrupting mitoribosome biogenesis and proteostasis.

This study identifies PknB-dependent phosphorylation of CslA as critical for cell wall morphogenesis in Streptomyces, showing how modulating β-glucan synthesis can counteract DivIVA dysregulation.

This study identifies and characterizes novel T6SS effectors in Chromobacterium violaceum, revealing RhsF as an antibacterial toxin with FIX and ADP-ribosyltransferase domains.

The paper introduces a pipeline for single-cell proteomics analysis that addresses challenges in data processing and annotation using context-aware methods and large language models.

The paper introduces Ubi-SCAPE, a method to purify poly-ubiquitylated proteins with high specificity, reducing contaminants and improving reproducibility.

The paper introduces a cost-effective single-cell proteomics method to analyze skin tumors in CYLD cutaneous syndrome, identifying a novel tumor-associated macrophage signature.

The paper identifies de novo truncating variants in XRN1's C-terminal region causing lethal infantile mitochondrial cardiomyopathy by disrupting its interaction with EDC4.

This study evaluates two mass spectrometry-based phenotypic screening approaches for identifying anti-inflammatory compounds in macrophages and compares them to cytokine profiling.

This study identifies Tfe2 as a novel antifungal effector that inhibits protein translation and hyperactivates TORC1, leading to cellular remodeling in yeast.

The paper identifies a distinct BAM complex in Bacteroidetes using structural biology and proteomics, revealing an expanded role compared to Proteobacteria.

The paper evaluates protein quantitation in DIA proteomics using controlled experiments on two mass spectrometry platforms, identifying over 10,000 proteins and highlighting the impact of post-processing on accuracy and false quantitative rates.

The paper develops a flow cytometry-based method combined with ultra-sensitive proteomics to study host-pathogen interactions in Salmonella-infected macrophages, revealing new insights into virulence factor induction and phagosomal dynamics.

The paper identifies CTDNEP1-NEP1R1 as the R-SMAD phosphatase and shows how its complex with MAN1 inactivates TGF-β signaling by dephosphorylating R-SMADs in the nucleus.

This study identifies non-canonical NF-κB signalling as a therapeutic target in CYLD cutaneous syndrome and shows that IKK inhibition reduces tumor viability in patient-derived models.

The paper compares proteomic profiles of murine macrophage cell lines to primary and immortalised bone marrow-derived macrophages, identifying J774A.1 as the most similar to primary cells.

This paper uses proteomics to show trilaciclib induces senescence in CML and NSCLC cells by stabilizing CDK4/6 and activating autophagy.

This study shows that a mutation in DNM1 causes epilepsy by disrupting synaptic vesicle endocytosis, and that a drug can reverse these effects in a mouse model.

This study identifies an ERK5-KLF2 signalling module that regulates 2C gene expression and mESC rejuvenation through both transcriptional activation and phosphorylation-induced degradation of KLF2.