Therese Dau

The paper identifies LMOD1 as a key regulator of myogenic differentiation through proteome dynamics and functional studies.

This paper identifies transient GSK3β activation as a mechanism promoting disease tolerance to sepsis through hypometabolism, without affecting pathogen burden.

This study compares molecular changes in PNS ageing, dietary restriction, and injury, finding similar proteomic signatures between ageing and injury.

This study shows YIPF5 regulates ER export of specific proteins, and its disruption causes neuronal migration defects and microcephaly.

The paper shows that IER3IP1 mutations cause microcephaly by blocking ER-Golgi transport, leading to neuronal migration defects and ER distension.

The paper investigates how LPS preconditioning affects microglial proteome response to focal ischemic brain injury in mice, finding significant neuroprotection and changes in proteome patterns linked to type I interferons.

The paper introduces an automated workflow for BioID to improve reproducibility and identification of protein-protein interactions by increasing throughput and reducing sample input requirements.