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Positional cloning uncovers mutations in PLCE1 responsible for a nephrotic syndrome variant that may be reversible
TLDR
These findings, together with the zebrafish model of human nephrotic syndrome generated by plce1 knockdown, open new inroads into pathophysiology and treatment mechanisms of nephrotsic syndrome. Expand
Podocin, a raft-associated component of the glomerular slit diaphragm, interacts with CD2AP and nephrin.
TLDR
It is shown, by immunoelectron microscopy, that podocin localizes to the podocyte foot process membrane, at the insertion site of the slit diaphragm, and it is postulate thatpodocin serves in the structural organization of the slat diaphagm and the regulation of its filtration function. Expand
Nephrin ectodomain engagement results in Src kinase activation, nephrin phosphorylation, Nck recruitment, and actin polymerization.
TLDR
The data support the model that during podocyte intercellular junction formation, engagement of the nephrin ectodomain induces transient catalytic activity that results in nephrine phosphorylation on specific nephin cytoplasmic domain tyrosine residues, which resulted in recruitment of the SH2-SH3 domain-containing adapter protein Nck and assembly of actin filaments in an Nck-dependent fashion. Expand
Wnt/beta-catenin signaling promotes podocyte dysfunction and albuminuria.
TLDR
The results suggest that targeting hyperactive Wnt/beta-catenin signaling may represent a novel therapeutic strategy for proteinuric kidney diseases, and upregulation of Wnt1 and active beta-Catenin in podocytes is observed. Expand
Fyn Binds to and Phosphorylates the Kidney Slit Diaphragm Component Nephrin*
TLDR
Results demonstrate that endogenous Fyn catalyzes Nephrin phosphorylation in podocyte detergent-resistant membrane fractions with Fyn and Yes, and the mechanism by which this occurs requires investigation. Expand
Recruitment of JNK to JIP1 and JNK-dependent JIP1 Phosphorylation Regulates JNK Module Dynamics and Activation*
TLDR
The present study corroborated the hypothesis that recruitment of JNK to JIP1 and phosphorylation of Jip1 by JNK is prerequisite for activation of the JNK module by demonstrating that JNK binding to J IP1 is necessary for stimulus-induced dissociation of DLK from JIP 1, for DLK oligomerization, and for JNK activation. Expand
Requirement for Ras/Rac1-Mediated p38 and c-Jun N-Terminal Kinase Signaling in Stat3 Transcriptional Activity Induced by the Src Oncoprotein
TLDR
It is demonstrated that Ras- and Rac1-mediated p38 and JNK signals are required for Stat3 transcriptional activity induced by the Src oncoprotein, delineating a network of tyrosine and serine/threonine kinase signaling pathways that converge on Stat3 in the context of oncogenesis. Expand
Tumor necrosis factor-alpha induction of novel gene products in human endothelial cells including a macrophage-specific chemotaxin.
TLDR
The production of a monocyte chemotaxin by cytokine-activated endothelium has important implications for understanding the role of the vessel wall in disease states such as atherosclerosis and may also in part explain the indirect angiogenic activity of TNF. Expand
Podocyte depletion and glomerulosclerosis have a direct relationship in the PAN-treated rat.
TLDR
This report supports the growing body of data linking glomerulosclerosis directly to a reduction in relative podocyte number [increased glomerular area per podocyte (GAPP)], and raises important questions related to the mechanisms of podocytes loss, strategies for prevention of podocyte depletion, and the prevention of progression of glomersular diseases. Expand
Protocadherin FAT1 binds Ena/VASP proteins and is necessary for actin dynamics and cell polarization
TLDR
Mammalian FAT1 is identified as a proximal element of a signaling pathway that determines both cellular polarity in the plane of the monolayer and directed actin‐dependent cell motility. Expand
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