Stephan Alexander Pless

This paper designs a deep learning-generated hASIC1a inhibitor that reduces infarct volume by over 50% in a mouse stroke model.

This study uses protein semi-synthesis and voltage-clamp fluorometry to track real-time conformational changes in the cardiac sodium channel NaV1.5 during inactivation.

This study presents cryo-EM structures of human ASIC1a across different pH levels and conditions, revealing conformational changes linked to channel function.

This study shows that NALCN deficiency preferentially affects GABAergic interneurons, reducing their intrinsic excitability and impairing contextual adaptation and spatial memory in mice.

The paper establishes a framework to assess NALCN variant pathogenicity using functional and computational methods, distinguishing benign from gain- and loss-of-function variants.

The paper identifies a functional interaction between ASIC1a and MCT1 that modulates proton sensitivity and desensitization, showing its role in glioblastoma cell survival and mouse lifespan.

The paper shows that SNARE complex proteins inhibit NALCN channel activity and that reducing NALCN currents promotes cell survival in syntaxin-depleted cells.

This study investigates conformational changes in ASIC1a under different desensitizing conditions using electrophysiology and fluorometry, revealing the role of the β11-12 linker in coupling ECD movements to the pore.

The paper identifies an unconventional conductance essential for pacemaking in nigral dopamine neurons using pharmacological evidence and electrophysiological analysis.

This paper introduces a method to insert synthetic peptides into proteins in eukaryotic cells to enable chemical modifications and non-canonical amino acids, validated using GFP, NaV1.5, and P2X2 receptors.

This paper identifies the functional requirements of the sodium leak channel complex and shows it is voltage-sensitive and modulated by extracellular calcium.