Julia Reichelt
Hamburg, HH 20246, Germany
Last Updated: 09/26/2026
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Found 9 publications
Autoantibody-triggered podocyte membrane budding drives autoimmune kidney disease.
Journal: Cell
Published: March 18, 2025
Regulation of podocyte surface proteins by the enzyme A Disintegrin And Metalloproteinase 10 (ADAM10).
Journal: Kidney international
Published: August 20, 2024
Publisher Correction: Non-functional ubiquitin C-terminal hydrolase L1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis.
Journal: Nature communications
Published: April 28, 2023
Non-functional ubiquitin C-terminal hydrolase L1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis.
Journal: Nature communications
Published: March 11, 2022
Tripartite Separation of Glomerular Cell Types and Proteomes from Reporter-Free Mice.
Journal: Journal of the American Society of Nephrology : JASN
Published: September 20, 2020
ADAM10-Mediated Ectodomain Shedding Is an Essential Driver of Podocyte Damage.
Journal: Journal of the American Society of Nephrology : JASN
Published: August 23, 2020
Ubiquitin C-terminal hydrolase L1 (UCH-L1) loss causes neurodegeneration by altering protein turnover in the first postnatal weeks.
Journal: Proceedings of the National Academy of Sciences of the United States of America
Published: March 30, 2019
Deubiquitinating Enzyme UCH-L1 Promotes Dendritic Cell Antigen Cross-Presentation by Favoring Recycling of MHC Class I Molecules.
Journal: Journal of immunology (Baltimore, Md. : 1950)
Published: August 16, 2018
Ubiquitin C-Terminal Hydrolase L1 is required for regulated protein degradation through the ubiquitin proteasome system in kidney.
Journal: Kidney international
Published: November 15, 2016
Showing 1-9 of 9
Last Updated: 09/26/2026