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Expression of -actinin-4 in acquired human nephrotic syndrome: a quantitative immunoelectron microscopy study
Author(s) -
N. P. Goode,
Mike Shires,
Tahir Naeem Khan,
Aisling Mooney
Publication year - 2004
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfg620
Subject(s) - immunoelectron microscopy , podocyte , nephrotic syndrome , microbiology and biotechnology , actin cytoskeleton , transmembrane protein , cytoskeleton , actin , medicine , signal transduction , renal glomerulus , phenotype , glomerulonephritis , immunology , biology , kidney , cell , genetics , gene , antibody , receptor , proteinuria
The molecular basis for the alteration of glomerular podocyte phenotype in nephrotic syndrome probably involves adaptive changes of the actin cytoskeleton. alpha-Actinin-4 is an actin cross-linking protein that also interacts with intra- and intercellular adhesion molecules and elements of the transmembrane signal transduction pathway and is implicated in nephrotic syndrome by animal models and human genetic studies.

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