Leszek Lisowski

This paper develops a hydrogel-based system to reprogram astrocytes into neurons by delivering reprogramming factors and valproic acid, enhancing neural repair.

This study shows AAV2 bypasses endosomal escape by using AAVR to access the trans-Golgi network, challenging the model of direct endosomal escape.

This study optimizes AAV serotypes and promoters to specifically target Muller glial cells in rats, identifying ShH10Y and GFAP promoter as the most effective combination for in vivo delivery.

This study optimizes AAV serotypes and promoters to specifically target Müller glial cells in rats, identifying ShH10Y and GFAP promoter as the most effective combination for in vivo delivery.

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

This study shows that maturing human cardiac organoids enhances disease modeling and drug discovery by mimicking in vivo development and enabling therapeutic testing for DSP cardiomyopathy.

This study characterizes the transcriptomic effects of Cas13bt3 in retinal cells and demonstrates its efficacy in silencing VEGFA mRNA in human retinal organoids and mouse models.

This study investigates how PSEN1 mutations in Alzheimer's disease affect neuronal excitability using iPSC-derived neurons and finds reduced excitability and altered Kv/Nav channel currents in mutant neurons.

ADEVO demonstrates a method to generate high-complexity adenovirus libraries for retargeting, showing improved replication and lysis in tumor cells.

This study evaluates AAV vectors in human liver explants under normothermic perfusion to assess their functionality and neutralization by human sera.

This study identifies a transient protein folding response in early TDP-43 disease that reduces aggregation, with DNAJB5 as a protective factor, and shows proteomic similarities between mouse and human TDP-43 proteinopathies.

The paper identifies UFMylation as a negative regulator of skeletal muscle function through proteome-wide systems genetics in mice and validates it in a disease model.