Non-functional ubiquitin c-terminal hydrolase l1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis

HIGHLIGHTS

• who: Julia Reichelt from the TSA-amplification, clone , Abcam) have published the research work: Non-functional ubiquitin C-terminal hydrolase L1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis, in the Journal: (JOURNAL) of 11/03/2022
• what: Converging biochemical, structural, mouse pathomechanistic, and clinical information the authors report that the deubiquitinase Ubiquitin C-terminal hydrolase L1 (UCH-L1) is induced by oxidative stress in podocytes and is directly involved in proteasome substrate accumulation.
• how: To assess whether UCH-L1 is rendered non-functional during experimental MN the authors made use of . . .
  

   

  

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