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Related Experiment Video

Updated: May 4, 2026

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USP40 protects podocytes by deubiquitylating integrin β1.

Naoaki Mikami1, Toshiaki Fukushima2, Hiromu Takematsu3

  • 1Department of Pediatrics, Kyorin University School of Medicine, Tokyo, Japan.

Biochemical and Biophysical Research Communications
|May 2, 2026
PubMed
Summary
This summary is machine-generated.

Ubiquitin-specific protease 40 (USP40) stabilizes podocyte adhesion by preventing integrin β1 internalization. Loss of USP40 worsens focal segmental glomerulosclerosis (FSGS) in mice, suggesting the USP40-integrin β1 pathway is a therapeutic target for FSGS.

Keywords:
DeubiquitylationFocal segmental glomerulosclerosisIntegrin β1PodocyteUbiquitin-specific protease 40 (USP40)

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Focal segmental glomerulosclerosis (FSGS) involves podocyte injury, but mechanisms remain unclear.
  • Podocyte detachment and loss are critical in FSGS pathogenesis.
  • Integrin β1 is vital for podocyte adhesion to the glomerular basement membrane.

Purpose of the Study:

  • To investigate the role of ubiquitin-specific protease 40 (USP40) in podocytes.
  • To determine USP40's effect on the adhesion molecule integrin β1.
  • To explore the USP40-integrin β1 axis as a potential therapeutic target for FSGS.

Main Methods:

  • Utilized USP40 knockout mice in an experimental FSGS model.
  • Performed USP40 knockdown in cultured podocytes.
  • Investigated integrin β1 ubiquitination and endocytosis in HEK293 cells and mouse podocytes.

Main Results:

  • USP40 knockout mice showed exacerbated proteinuria, glomerulosclerosis, and reduced podocyte number and integrin β1 expression.
  • USP40 knockdown in podocytes decreased integrin β1 expression and impaired cell adhesion.
  • USP40 suppressed integrin β1 monoubiquitylation and prevented its clathrin-mediated endocytosis.

Conclusions:

  • USP40 stabilizes integrin β1 at the podocyte plasma membrane by inhibiting its endocytosis.
  • The USP40-integrin β1 pathway is crucial for maintaining podocyte adhesion.
  • Targeting the USP40-integrin β1 axis may offer a novel therapeutic strategy for FSGS.