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  1. Article

    Open Access

    Publisher Correction: Non-functional ubiquitin C-terminal hydrolase L1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis

    Julia Reichelt, Wiebke Sachs, Sarah Frömbling, Julia Fehlert in Nature Communications (2023)

  2. Article

    Open Access

    Non-functional ubiquitin C-terminal hydrolase L1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis

    Little is known about the mechanistic significance of the ubiquitin proteasome system (UPS) in a kidney autoimmune environment. In membranous nephropathy (MN), autoantibodies target podocytes of the glomerular...

    Julia Reichelt, Wiebke Sachs, Sarah Frömbling, Julia Fehlert in Nature Communications (2023)

  3. Article

    Open Access

    The classical pathway triggers pathogenic complement activation in membranous nephropathy

    Membranous nephropathy (MN) is an antibody-mediated autoimmune disease characterized by glomerular immune complexes containing complement components. However, both the initiation pathways and the pathogenic si...

    Larissa Seifert, Gunther Zahner, Catherine Meyer-Schwesinger in Nature Communications (2023)

  4. Article

    Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1

    Acute glomerulonephritis can lead to chronic glomerulonephritis or resolve without permanent damage to the kidneys. Differential gene expression was studied in a model of acute and chronic glomerulonephritis t...

    Claudia Jafari, Ulf Panzer, Oliver M. Steinmetz in Cellular & Molecular Biology Letters (2006)