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Trophoblast Glycoprotein: Possible Candidate Mediating Podocyte Injuries in Glomerulonephritis
Author(s) -
Taichi Murakami,
Hideharu Abe,
Kojiro Nagai,
Tatsuya Tominaga,
Norimichi Takamatsu,
Toshikazu Araoka,
Seiji Kishi,
Tomohiro Takahashi,
Akira Mima,
Yoshimi Takai,
Jeffrey B. Kopp,
Toshio Doi
Publication year - 2010
Publication title -
american journal of nephrology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.394
H-Index - 85
eISSN - 1421-9670
pISSN - 0250-8095
DOI - 10.1159/000321366
Subject(s) - podocyte , microbiology and biotechnology , podocalyxin , cytochalasin d , focal adhesion , rhoa , cytoskeleton , gene knockdown , downregulation and upregulation , small interfering rna , biology , transfection , endocrinology , kidney , cell , cell culture , signal transduction , genetics , proteinuria , biochemistry , gene
trophoblast glycoprotein (Tpbg), a 72-kDa transmembrane glycoprotein, is known to regulate the phenotypes of epithelial cells by modifying actin organization and cell motility. Recently, a microarray study showed that Tpbg is upregulated in Thy1 glomerulonephritis (Thy1 GN). We hypothesized that Tpbg regulates cytoskeletal rearrangement and modulates phenotypic alteration in podocytes under pathological conditions.

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