Alexander Schmidt

This study identifies distinct subpopulations of Pseudomonas aeruginosa that use different virulence factors to cause tissue damage during infection.

SPEx enables compartment-resolved proteomics by expanding cells, microdissecting regions of interest, and analyzing them with mass spectrometry, revealing novel organelle components.

The paper identifies a nucleolus-like condensate in E. coli that forms during cold adaptation to enhance ribosome biogenesis.

The paper develops a computational method to deconvolve cell cycle-dependent protein dynamics from bulk proteomics data in budding yeast and identifies 563 proteins with such dynamics.

This study shows that H6PD deficiency in mice leads to increased hepatic triglycerides and lipid accumulation, linking NADPH availability to fatty acid homeostasis.

This paper identifies a distinct HCC subgroup defined by high regeneration-associated stress, showing vulnerability to ATR inhibitors and proposing LIVRESS as a biomarker for treatment stratification.

This paper shows that extracellular vesicles contaminate nanoparticle protein corona profiles in human plasma, leading to inaccurate protein origin assignments.

This paper identifies a stage-specific proteomic signature of Alzheimer's disease using plasma proteomics and finds a proteomic switch associated with disease progression.

This study uses cryo-electron tomography to show vault particles associate with ER and nuclear envelope membranes and enclose ribosomes in Dictyostelium discoideum.

This paper identifies NaR as a liver clock-controlled metabolite that links circadian rhythms to adipogenesis via the prefoldin complex and UPR signaling.

This study shows that mobile genetic elements in bacteria generate antibiotic persistence traits through heterogeneous chromosomal excision, enhancing survival under antibiotic treatment.

This study identifies Pfk2p as an ATP-dependent RNA unwinding enzyme that modulates cell cycle progression by promoting translation of mitotic genes.

This study uses ribosome profiling to show that steatohepatitis-associated HCC has extensive translational alterations affecting hundreds of genes and revealing novel translated regions.

This study identifies DRP1 and Ca2+ as essential for endocytic lysosome reformation by mediating tubule fission at ER-mitochondria-endolysosome contact sites.

The paper identifies and functionally characterizes a novel cis-regulatory element, apLSE, essential for hindgut morphogenesis and adult survival in Drosophila melanogaster.

This study identifies coenzyme A depletion as a cause of antibiotic tolerance in Pseudomonas aeruginosa using proteomic, metabolomic, and machine learning analyses.

The paper shows that bacterial-derived RNA extends healthspan in C. elegans by reducing protein aggregation through inter-tissue communication and systemic RNAi.

The paper shows that epistatic interactions between RpoB and GyrA mutations in Mycobacterium tuberculosis can lead to high-fitness double-resistant strains, which are prevalent in clinical isolates.

This study genetically validates PfFKBP35 as a lethal target in Plasmodium falciparum, showing its role in ribosome homeostasis and revealing non-canonical modes of action for FK506.

This study identifies RPL39L as an efficiency factor in cotranslational folding of alpha helical proteins by analyzing its expression, ribosome structure, and impact on translation dynamics.

This study identifies transcription factor networks involved in hepatocyte lipotoxicity using integrative transcriptomic, proteomic, and chromatin accessibility analyses, showing that MAFK and TCF4 deletion protects against fatty acid toxicity.

This study reveals that RNA-bound PGC-1α forms liquid-like nuclear condensates to regulate gene expression and transcriptional networks in response to metabolic stimuli.

The paper develops a synthetic biosensor to measure glycolytic flux in single yeast cells using fluorescence microscopy to identify metabolic subpopulations.

This study shows that mTORC1 inhibition in adult mice does not cause muscle atrophy or functional decline, despite metabolic and morphological changes.