Kathrin Textoris‐Taube

The paper shows that alpha-synuclein phase separation can form Lewy body-like structures without pre-existing seeds, suggesting a new mechanism for neurodegeneration.

The paper creates a proteoform-resolved atlas of the human plasma proteome, revealing extensive proteoform diversity and highlighting discrepancies between proteomic platforms.

The paper investigates how anesthetic exposure affects brain energy metabolism in an Alzheimer's model, showing reduced oxidative metabolism and worsened potassium regulation in diseased tissue.

The paper shows lipid chlorination by MPO-derived hypochlorous acid enables NE release from granules, initiating NETosis.

This study identifies HLA-I peptides and their source proteins from Sezary Syndrome patients to uncover potential T-cell immunotherapeutic targets.

This study shows that liver viscosity decreases before fibrosis in a mouse model of MASH, indicating it as a potential early biomarker.

This study uses proteomics to analyze glucose-stimulated insulin secretion in rat beta cells, finding that fatty acid metabolism plays a key role in the process.

This study identifies DTX4 as a regulator of neural progenitor transitions during cortical development, showing its role in maintaining radial glia identity and preventing intermediate progenitor generation.

The paper quantifies proteomic effects of aneuploidy in natural yeast isolates, finding chromosome-wide dosage compensation in the proteome but not transcriptome.

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.

The paper identifies that tyrosine halogenation of α-defensins by hypohalous acids converts them into immunomodulatory mediators, revealing a novel oxidative mechanism in neutrophil function.

The paper shows that Sema7A and Sema4D heterodimerization is essential for membrane targeting and neocortical wiring, with a mutation in Sema4D causing epilepsy.