Wolfgang Wurst

This study identifies RNF126 as a ubiquitin ligase involved in lysosomal damage response and homeostasis, showing its recruitment to lysosomes and role in substrate ubiquitylation.

The paper develops new mouse reporter models to detect genome editing events in vivo, including gene repair and CRISPR indels, and A-base editor activity.

This study shows that DJ-1 deficiency impairs VMAT2 function and vesicle dynamics, leading to dopamine oxidation and α-synuclein pathology in Parkinson's disease neurons.

This study investigates how TREM2 expression levels affect microglial function, metabolism, and response to TREM2 agonists in a mouse model of Alzheimer's disease.

GluTrooper is a mouse line for whole-brain glutamate imaging with long-lasting sensor expression and multimodal imaging capabilities.

This study shows that extracellular alpha-synuclein toxicity in Parkinson's disease is independent of intracellular alpha-synuclein and linked to mitochondrial dysfunction.

The paper reports the generation of over 5,000 new mouse mutant strains for targeted genes, significantly expanding the available genetic resources for biomedical research.

This study shows that SERF2 deletion changes amyloid fibril structure in Alzheimer's mouse models, suggesting SERF's role in modifying amyloid aggregation.

This study identifies a protective Plcγ2-P522R variant in Alzheimer's disease by showing it enhances microglial functions like phagocytosis and survival.

The paper integrates gene essentiality data from human and mouse screens to classify genes into FUSIL categories, identifying developmental lethal genes associated with rare diseases.

This study shows that canonical Wnt/{beta}-catenin signaling modulates the timing and progression of dendritic growth in adult-born hippocampal neurons, with distinct effects in young and aged mice.

This study identifies PINK1's role in regulating mitochondrial function, lipid metabolism, and dopamine homeostasis in dopaminergic neurons, showing that cholesterol depletion can reverse PINK1-related phenotypes.

The paper introduces a method called soft windowing to improve analysis of high-throughput phenotyping data by reducing false positives and increasing significant results.