This study investigates the role of UCH-L1 in podocyte injury within the context of autoimmune glomerulonephritis. The researchers demonstrate that oxidative stress induces the expression of a non-functional form of UCH-L1 in podocytes, which impairs proteasome activity, leading to protein accumulation and cell injury. Podocyte-specific deletion of UCH-L1 mitigates these effects, highlighting its pathogenic role.
Oxidative stress induces non-functional UCH-L1 expression in podocytes, impairing proteasome function and leading to protein accumulation and cell injury. Podocyte-specific deletion of UCH-L1 protects against these effects, underscoring its role in disease pathogenesis.
UCHL1(fl/fl) conditional Knockout mouse model developed by genOway, allowing for tissue-specific deletion of UCHL1 to study its function in podocyte biology and glomerular disease.
Autoimmune glomerulonephritis, Podocyte injury, Proteasome dysfunction, Oxidative stress, Ubiquitin-proteasome system
Conditional Knockout model, LoxP-flanked UCHL1 alleles, Tissue-specific Cre recombinase, Oxidative stress assays, Proteasome activity measurements
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
