Afadin is localized at cell-cell contact sites in mesangial cells and regulates migratory polarity.

ABSTRACT: In kidney glomeruli, mesangial cells provide structural support to counteract for expansile forces caused by pressure gradients and to regulate the blood flow. Glomerular injury results in proliferation and aberrant migration of mesangial cells, which is the pathological characteristic of mesangial proliferative glomerulonephritis. To date, molecular changes that occur in mesangial cells during glomerular injury and their association with the pathogenesis of glomerulonephritis remain largely unclear. During the search for proteins regulating the morphology of mesangial cells, we found that afadin, a multi-domain F-actin-binding protein, and β-catenin are expressed in cell-cell contact sites of cultured mesangial cells and mesangial cells in vivo. Afadin forms a protein complex with β-caten

SUBMITTER: Tsurumi H 

PROVIDER: S-EPMC5399166 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature