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Marlies Sachs

University of Hamburg

16

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280

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ADAM10-Mediated Ectodomain Shedding Is an Essential Driver of Podocyte Damage.

2021 Journal of The American Society of Nephrology
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Ubiquitin C-terminal hydrolase L1 (UCH-L1) loss causes neurodegeneration by altering protein turnover in the first postnatal weeks

2019 Proceedings of the National Academy of Sciences of the United States of America
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Deubiquitinating Enzyme UCH-L1 Promotes Dendritic Cell Antigen Cross-Presentation by Favoring Recycling of MHC Class I Molecules

2019 Journal of Immunology
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Ubiquitin C-Terminal Hydrolase L1 is required for regulated protein degradation through the ubiquitin proteasome system in kidney

2018 Kidney International
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MicroRNA-193a Regulates the Transdifferentiation of Human Parietal Epithelial Cells toward a Podocyte Phenotype

2015 Journal of The American Society of Nephrology
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Glomerulopathy Induced by Immunization with a Peptide Derived from the Goodpasture Antigen α3IV-NC1

2015 Journal of Immunology
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Alterations in the Ubiquitin Proteasome System in Persistent but Not Reversible Proteinuric Diseases

2014 Journal of The American Society of Nephrology
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Characterization of the renal CD4+ T-cell response in experimental autoimmune glomerulonephritis

2012 Kidney International
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Ubiquitin C-Terminal Hydrolase-L1 Activity Induces Polyubiquitin Accumulation in Podocytes and Increases Proteinuria in Rat Membranous Nephropathy

2011 American Journal of Pathology
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Citations (37)