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anti-Human Nephrin Antibodies:
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Human Polyclonal Nephrin Primary Antibody for IF, IHC (p) - ABIN113479
Huber, Hartleben, Winkelmann, Schneider, Becker, Leitges, Walz, Haller, Schiffer: Loss of podocyte aPKClambda/iota causes polarity defects and nephrotic syndrome. in Journal of the American Society of Nephrology : JASN 2009
Show all 13 references for ABIN113479
Human Polyclonal Nephrin Primary Antibody for EIA, IF - ABIN500330
Kestilä, Lenkkeri, Männikkö, Lamerdin, McCready, Putaala, Ruotsalainen, Morita, Nissinen, Herva, Kashtan, Peltonen, Holmberg, Olsen, Tryggvason: Positionally cloned gene for a novel glomerular protein--nephrin--is mutated in congenital nephrotic syndrome. in Molecular cell 1998
Show all 3 references for ABIN500330
Human Polyclonal Nephrin Primary Antibody for ELISA, ICC - ABIN4338586
Motiram Kakalij, Tejaswini, Patil, Dinesh Kumar, Diwan: Vanillic Acid Ameliorates Cationic Bovine Serum Albumin Induced Immune Complex Glomerulonephritis in BALB/c Mice. in Drug development research 2016
Mouse (Murine) Polyclonal Nephrin Primary Antibody for FACS, IF (p) - ABIN669501
Sun, Qu, Howard, Dai, Jiang, Ren, Fu, Puelles, Nikolic-Paterson, Caruana, Bertram, Sleeman, Li: Smad3 deficiency protects mice from obesity-induced podocyte injury that precedes insulin resistance. in Kidney international 2015
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.
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.
biochemical reconstitution on supported lipid bilayers of protein clusters containing the adhesion receptor Nephrin and its cytoplasmic partners, Nck (show NCK1 Antibodies) and N-WASP (show WASL Antibodies), is reported.
Coding variants in NPHS1 are associated with both risk for and protection from common forms of nephropathy in African Americans.
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 Antibodies)) is involved in insulin (show INS Antibodies) 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 Antibodies) deficiency exacerbates kidney inflammation, oxidative stress and adverse renal injury in the ApoE (show APOE Antibodies)-mutant mice through modulation of the nephrin, NOX4 (show NOX4 Antibodies) and TNF-alpha (show TNF Antibodies)-TNFRSF1A (show TNFRSF1A Antibodies) signaling.
Nephrin is involved in pancreatic beta-cell survival signaling; a marked decrease in nephrin expression and phosphorylated Akt (show AKT1 Antibodies) was observed in pancreatic islets of leptin receptor (show LEPR Antibodies)-deficient diabetic mice.
SHP-1 (show PTPN6 Antibodies) contributes to nephrin deactivation in podocytes exposed to high glucose levels.
The aPKC-Par3 (show F2RL2 Antibodies) complex regulates the cell-surface localization of nephrin.
A novel direct interaction between the Sema3a (show SEMA3A Antibodies) signaling receptor plexinA1 (show PLXNA1 Antibodies) and nephrin, linking extracellular Sema3a (show SEMA3A Antibodies) signals to the slit-diaphragm signaling complex, was identified.
The planar cell polarity pathway contributes to podocyte development by regulating nephrin turnover during junctional remodeling as the cells differentiate.
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