Christian Griesinger

The paper shows that the disordered C-terminal segment of Skp1, H8, nucleates helices but limits their propagation through a charge-sensitive rheostat, maintaining conformational flexibility.

Anle138b reduces mHTT aggregates and improves disease phenotypes in HD cell and mouse models.

The paper characterizes the multi-timescale structural dynamics of the p53 transactivation domain using NMR and simulations, revealing a hierarchical energy landscape.

This paper shows that anle138b binds to a cavity in lipidic Aβ fibrils and reduces fibril formation by 75%, suggesting a potential therapeutic mechanism for Alzheimer's disease.

This study identifies two binding sites of the PET tracer MODAG-005 on lipidic α-synuclein fibrils, with the cavity site being more stable and selectively occupied under certain conditions.

The paper investigates the transmembrane signaling mechanism of the CitA histidine kinase using structural biology techniques and shows how structural changes in the sensor domain are transmitted across the membrane.

This study shows that anle138b reduces hyperglycemia and improves pancreatic islet function in hIAPP Ob/Ob mice by mitigating hIAPP toxicity.

The paper determines the structure of amyloid-β (Aβ40) fibrils bound to lipids using cryo-EM, showing lipid binding and potential relevance to Alzheimer's disease pathogenesis.

The paper presents six atomic structures of α-synuclein fibrils in the presence of phospholipids, revealing how phospholipids influence fibril morphology and lipid interactions.

The paper evaluates pharmacological modulators of α-synuclein and tau aggregation and internalization, identifying compounds that reduce their aggregation and spread.

This study develops a new Parkinson's disease mouse model showing that reducing α-synuclein aggregates rescues dopamine neuron dysfunction and death.