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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.
Mutation analysis showed that each patient carried a compound heterozygous mutation of NPHS1 gene. Patient 1 carried IVS 24 + 5 G > A and c2663G > A (p.R888K) mutations (Figs. 1 and 2). Patient 2 carried IVS6-1G > C and c1760T > G (p.L587R) mutations (Figs. 3 and 4). Each mutation was inherited from paternal and maternal DNA respectively.
Angiotensin II has a role in increasing glomerular permeability by beta-arrestin mediated nephrin endocytosis
This prospective observational study compare urine nephrin:creatinine ratio (NCR, ng/mg) with serum soluble fms-like tyrosine kinase-1 (zeige FLT1 Proteine):placental growth factor (zeige PGF Proteine) ratio (FPR (zeige FPR1 Proteine), pg/pg) for preeclampsia (PE) prediction among unselected asymptomatic pregnant women in 2(nd) trimester.
Outcomes of renal replacement therapy in NPHS1 patients in Europe were analysed using data from the ESPN (zeige ESPN Proteine)/ERA-EDTA Registry
WHSC1L1 (zeige WHSC1L1 Proteine)-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.
Here, we found the dynamic changes of Notch1 (zeige NOTCH1 Proteine) were coincided with autophagy: they both increased during kidney development and podocyte differentiation...to better understand the relationship between Notch (zeige NOTCH1 Proteine) signalling and autophagy in podocyte differentiation, rapamycin was added to enhance autophagy levels in DAPT-treated cells, and as a result, nephrin was recovered and DAPT-induced injury was ameliorated
Data (including data from studies using transgenic mice, an murine experimental model of diabetes, and mouse/human cell lines) suggest prostaglandin I2 receptor (Ptgir (zeige PTGIR Proteine)) is involved in insulin (zeige INS Proteine) 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 (zeige ACE2 Proteine) deficiency exacerbates kidney inflammation, oxidative stress and adverse renal injury in the ApoE (zeige APOE Proteine)-mutant mice through modulation of the nephrin, NOX4 (zeige NOX4 Proteine) and TNF-alpha (zeige TNF Proteine)-TNFRSF1A (zeige TNFRSF1A Proteine) signaling.
Nephrin is involved in pancreatic beta-cell survival signaling; a marked decrease in nephrin expression and phosphorylated Akt (zeige AKT1 Proteine) was observed in pancreatic islets of leptin receptor (zeige LEPR Proteine)-deficient diabetic mice.
SHP-1 (zeige PTPN6 Proteine) contributes to nephrin deactivation in podocytes exposed to high glucose levels.
The aPKC-Par3 (zeige F2RL2 Proteine) complex regulates the cell-surface localization of nephrin.
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