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anti-Human Nephrin Antikörper:
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Human Polyclonal Nephrin Primary Antibody für 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 Pubmed References
Human Polyclonal Nephrin Primary Antibody für IHC, ELISA - ABIN1002884
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 Pubmed References
Human Polyclonal Nephrin Primary Antibody für 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
Show all 2 Pubmed References
Mouse (Murine) Polyclonal Nephrin Primary Antibody für IF (p), IHC (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
Human Polyclonal Nephrin Primary Antibody für IF (p), IHC (p) - ABIN2177857
Chen, Cheng, Chen, Shao, Sung, Chiang, Yang, Lin, Sun, Sheu, Chang, Lee, Yip: Combination therapy of exendin-4 and allogenic adipose-derived mesenchymal stem cell preserved renal function in a chronic kidney disease and sepsis syndrome setting in rats. in Oncotarget 2018
Human Polyclonal Nephrin Primary Antibody für IF (p) - ABIN2177861
Fu, Guo, Wang, Huang, Jin, Hu, Chen, Xu, Zhou, Zhao, Sung, Wang, Gaskin, Yang, Fu: Podocyte Activation of NLRP3 Inflammasomes Contributes to the Development of Proteinuria in Lupus Nephritis. in Arthritis & rheumatology (Hoboken, N.J.) 2017
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 (zeige ESPN Antikörper)/ERA-EDTA Registry
WHSC1L1 (zeige WHSC1L1 Antikörper)-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.
Here, we found the dynamic changes of Notch1 (zeige NOTCH1 Antikörper) were coincided with autophagy: they both increased during kidney development and podocyte differentiation...to better understand the relationship between Notch (zeige NOTCH1 Antikörper) 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 Antikörper)) is involved in insulin (zeige INS Antikörper) 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 Antikörper) deficiency exacerbates kidney inflammation, oxidative stress and adverse renal injury in the ApoE (zeige APOE Antikörper)-mutant mice through modulation of the nephrin, NOX4 (zeige NOX4 Antikörper) and TNF-alpha (zeige TNF Antikörper)-TNFRSF1A (zeige TNFRSF1A Antikörper) signaling.
Nephrin is involved in pancreatic beta-cell survival signaling; a marked decrease in nephrin expression and phosphorylated Akt (zeige AKT1 Antikörper) was observed in pancreatic islets of leptin receptor (zeige LEPR Antikörper)-deficient diabetic mice.
SHP-1 (zeige PTPN6 Antikörper) contributes to nephrin deactivation in podocytes exposed to high glucose levels.
The aPKC-Par3 (zeige F2RL2 Antikörper) 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