Matthias C. Truttmann

This study shows that FICD modulates dopamine receptor dynamics in neurons, affecting motivated behavior in Drosophila, C. elegans, and mice.

This study shows that loss of FICD rescues motor impairments and reverses oligodendrocyte maturation deficits in a SCA3 mouse model by restoring ER homeostasis and myelination.

This study shows that HSF1 forms stress-induced condensates with divergent transcriptional outcomes, impacting transcriptional responses during different stress conditions.

This study develops two nanobodies that specifically target HSP-1, reducing its ATPase activity and protein folding capacity both in vitro and in vivo.

This study shows that FICD deficiency protects mice from heart failure by enhancing BiP-mediated UPRER and ER-phagy under stress.

This study shows that loss of FIC-1-mediated AMPylation activates the UPRER and increases cytosolic HSP70 chaperones, which reduces polyglutamine toxicity in C. elegans.

This study identifies two small molecule inhibitors of FICD that suppress both endogenous and pathologic protein AMPylation, improving proinsulin processing in β cells.

This study shows how two HSP70 chaperones in C. elegans, HSP-3 and HSP-4, have distinct and overlapping roles in ER proteostasis, affecting growth, reproduction, stress resistance, aging, and ER-Phagy.

This study shows that C. elegans uses AWB and ASH neurons to detect dead conspecifics, triggering behaviors that prioritize reproduction over lifespan.

TSWIFT enables iterative staining of mounted FFPE brain sections for high-dimensional proteome analysis.

This study shows that deleting mFICD in mice affects cytokine secretion and improves cognitive plasticity in older mice.