ArticleThe American journal of pathology2011
Phosphorylation of podocalyxin (Ser415) Prevents RhoA and ezrin activation and disrupts its interaction with the actin cytoskeleton.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Role of Rho GTPase Interacting Proteins in Subcellular Compartments of Podocytes.International journal of molecular sciences · 2021Review
- Cold Saline Perfusion before Ischemia-Reperfusion Is Harmful to the Kidney and Is Associated with the Loss of Ezrin, a Cytoskeletal Protein, in Rats.Biomedicines · 2021Article
- Coro2b, a podocyte protein downregulated in human diabetic nephropathy, is involved in the development of protamine sulphate-induced foot process effacement.Scientific reports · 2019Article
- Loss of ezrin expression reduced the susceptibility to the glomerular injury in mice.Scientific reports · 2018Article
- Loss of podocalyxin causes a novel syndromic type of congenital nephrotic syndrome.Experimental & molecular medicine · 2017Article
- Podocalyxin influences malignant potential by controlling epithelial-mesenchymal transition in lung adenocarcinoma.Cancer science · 2017Article
- The cell surface mucin podocalyxin regulates collective breast tumor budding.Breast cancer research : BCR · 2016Article
- Podocytes.F1000Research · 2016Review
- A molecular switch for the orientation of epithelial cell polarization.Developmental cell · 2014Article
- GIV/Girdin is a central hub for profibrogenic signalling networks during liver fibrosis.Nature communications · 2014Article
- Exome sequencing and in vitro studies identified podocalyxin as a candidate gene for focal and segmental glomerulosclerosis.Kidney international · 2014Article
- Prohibitin-2 binding modulates insulin-like growth factor-binding protein-6 (IGFBP-6)-induced rhabdomyosarcoma cell migration.The Journal of biological chemistry · 2013Article
- Ezrin Orchestrates Signal Transduction in Airway Cells.Reviews of physiology, biochemistry and pharmacologyReview
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Podocalyxin (PC) is a polysialylated, anti-adhesin that is essential for maintaining foot process architecture and the integrity of the glomerular filtration barrier. We showed previously that PC is firmly attached to the actin cytoskeleton through ezrin, that in puromycin aminonucleoside (PAN)-mediated nephrosis the PC-ezrin-actin complex is disrupted, and that PC is uncoupled from actin. However, the precise mechanisms involved remained unknown. Here we show that detachment of PC from actin is regulated by phosphorylation of PC. PC is hyperphosphorylated at serines in PAN- and protamine sulfate (PS)-treated rat glomeruli. We determined that PC is a substrate of PKC and that the site of phosphorylation is Ser415, located within the juxtamembrane, ezrin-binding domain of the cytoplasmic tail of PC. Mutation of Ser415 to the phosphomimetic residues Glu (S415E) or Asp (S415D) interfered with direct binding of the PC cytoplasmic tail to ezrin in vitro. Moreover, stable expression of a phosphomimetic (S415E) PC mutant but not the WT or the phosphorylation-deficient (S415A) PC mutant, disrupted PC-ezrin-actin interaction, failed to activate RhoA, and the cytoskeletal linker, ezrin, remained inactive. Our data indicate that phosphorylation of PC at Ser415 prevents attachment of PC and ezrin to actin and highlights the strategic position of Ser415 and direct binding of PC to ezrin in regulating podocyte foot process architecture.
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