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zApoL1 is essential for proper blood filtration in the zebrafish glomerulus and that zApoL1 affects the expression of nephrin
Nephrin signal bordered the lateral membrane of podocytes, which were columnar in shape
Using two models, zebrafish and mice, that the absence of nephrin results in poorly developed muscles and incompletely fused myotubes, respectively.
Outcomes of renal replacement therapy in NPHS1 patients in Europe were analysed using data from the ESPN (show ESPN Proteins)/ERA-EDTA Registry
WHSC1L1 (show WHSC1L1 Proteins)-L acts as a histone methyltransferase in podocytes and regulates nephrin gene expression, which may in turn contribute to the integrity of the slit diaphragm of the glomerular filtration barrier.
Two novel putatively deleterious NPHS1 variants were identified in children with steroid-resistant nephrotic syndrome.
On genetic analysis of NPHS1 a paternally derived heterozygous frame-shift mutation caused by an 8 bp deletion, resulting in a stop codon in exon 16 (c.2156-2163 delTGCACTGC causing p.L719DfsX4), and a novel, maternally derived nonsense mutation in exon 15 (c.1978G>T causing p.E660X) were identified.
Case Reports: NPHS1 mutations in four Brazilian cases of congenital nephrotic syndrome.
The classical form is CNF, which is caused by mutations in the nephrin gene (NPHS1), leading to massive proteinuria, hypoproteinemia and edema in the newborn period
there is a link found of the glomerular protein nephrin and the antihypertensive action of angiotensin receptor antagonists in the treatment of hypertension.
A novel nonsense mutation in NPHS1 linking aortic stenosis associated with congenital nephropathy, is reported.
Activated IQGAP1, as an intracellular partner of nephrin, is involved in actin cytoskeleton organization and functional regulation of podocytes.
NPHS1 rs437168 variant is associated with nephrotic syndrome in children.
Data (including data from studies using transgenic mice, an murine experimental model of diabetes, and mouse/human cell lines) suggest prostaglandin I2 receptor (Ptgir (show PTGIR Proteins)) is involved in insulin (show INS Proteins) secretion in pancreatic beta-cells and in permselectivity in glomerular podocytes; the mechanism appears to involve regulation of post-translational phosphorylation of nephrin.
the interaction between nephrin and MAGI-1 regulates Rap1 activation in podocytes to maintain long term slit diaphragm structure
interaction of full-length suPAR with alphavbeta3 integrin expressed on podocytes results in down-modulation of nephrin that may affect kidney functionality in different human pathologies characterized by increased concentration of suPAR.
Nphs1 is an activity dependent gene in mouse olfactory sensory neurons.
ACE2 (show ACE2 Proteins) deficiency exacerbates kidney inflammation, oxidative stress and adverse renal injury in the ApoE (show APOE Proteins)-mutant mice through modulation of the nephrin, NOX4 (show NOX4 Proteins) and TNF-alpha (show TNF Proteins)-TNFRSF1A (show TNFRSF1A Proteins) signaling.
Nephrin is involved in pancreatic beta-cell survival signaling; a marked decrease in nephrin expression and phosphorylated Akt (show AKT1 Proteins) was observed in pancreatic islets of leptin receptor (show LEPR Proteins)-deficient diabetic mice.
SHP-1 (show PTPN6 Proteins) contributes to nephrin deactivation in podocytes exposed to high glucose levels.
The aPKC-Par3 (show F2RL2 Proteins) complex regulates the cell-surface localization of nephrin.
A novel direct interaction between the Sema3a (show SEMA3A Proteins) signaling receptor plexinA1 (show PLXNA1 Proteins) and nephrin, linking extracellular Sema3a (show SEMA3A Proteins) signals to the slit-diaphragm signaling complex, was identified.
This gene encodes a member of the immunoglobulin family of cell adhesion molecules that functions in the glomerular filtration barrier in the kidney. The gene is primarily expressed in renal tissues, and the protein is a type-1 transmembrane protein found at the slit diaphragm of glomerular podocytes. The slit diaphragm is thought to function as an ultrafilter to exclude albumin and other plasma macromolecules in the formation of urine. Mutations in this gene result in Finnish-type congenital nephrosis 1, characterized by severe proteinuria and loss of the slit diaphragm and foot processes.
nephrosis 1, congenital, Finnish type (nephrin)
, renal glomerulus-specific cell adhesion receptor
, nephrosis 1 homolog, nephrin
, nephrin 1