Nephrin
Mostrando 1-12 de 35 artigos, teses e dissertações.
-
1. Nephrin gene expression in chronic kidney disease of dogs with Leishmania (Leishmania) infantum chagasi
Braz J Infect Dis. Publicado em: 2016-10
-
2. Expressão gênica de moléculas associadas ao podócito em pacientes portadores de glomerulopatias proteinúricas
Introdução: A injúria ao podócito glomerular tem um papel crítico para o surgimento de proteinúria em diferentes glomerulopatias. Neste estudo avaliamos a expressão gênica das proteínas associadas ao podócito em biópsias renais e na urina simultaneamente em pacientes com glomerulopatias proliferativas (GPP) e não proliferativas (GPNP) proteinúri
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 2012
-
3. Early renal abnormalities in a experimental model that combind genetic arterial hypertension and diabetes mellitus : effect of anty-hypertensive treatment / Alterações renais precoces em um modelo experimental que combina hipertensão arterial genetica e diabetes mellitus : efeitos do tratamento anti-hipertensivo
In diabetic patients hypertension is the main secondary factor associated with the development and progression of renal disease. However, the mechanism of interaction between diabetes and hypertension to exacerbate diabetic renal disease is poorly understood. The aim of this study was to evaluate the effect of presence of hypertension had on nephrin expressi
Publicado em: 2006
-
4. Nephrin is specifically located at the slit diaphragm of glomerular podocytes
We describe here the size and location of nephrin, the first protein to be identified at the glomerular podocyte slit diaphragm. In Western blots, nephrin antibodies generated against the two terminal extracellular Ig domains of recombinant human nephrin recognized a 180-kDa protein in lysates of human glomeruli and a 150-kDa protein in transfected COS-7 cel
The National Academy of Sciences.
-
5. Nephritogenic mAb 5-1-6 is directed at the extracellular domain of rat nephrin
mAb 5-1-6 identifies an antigen on rat podocyte slit-diaphragms and induces severe proteinuria when injected into rats. Nephrin, an Ig-like transmembrane protein that is mutated in congenital nephrotic syndrome of the Finnish type, has been localized to the slit-diaphragm on human podocytes. Here we document that the mAb 5-1-6 antigen is rat nephrin. After i
American Society for Clinical Investigation.
-
6. Cell junction-associated proteins IQGAP1, MAGI-2, CASK, spectrins, and α-actinin are components of the nephrin multiprotein complex
Nephrin is a cell surface receptor of the Ig superfamily that localizes to slit diaphragms, the specialized junctions between the interdigitating foot processes of the glomerular epithelium (podocytes) in the kidney. Mutations in the NPHS1 gene encoding nephrin lead to proteinuria and congenital nephrotic syndrome, indicating that nephrin is essential for no
National Academy of Sciences.
-
7. Nephrin strands contribute to a porous slit diaphragm scaffold as revealed by electron tomography
Nephrin is a key functional component of the slit diaphragm, the structurally unresolved molecular filter in renal glomerular capillaries. Abnormal nephrin or its absence results in severe proteinuria and loss of the slit diaphragm. The diaphragm is a thin extracellular membrane spanning the approximately 40-nm-wide filtration slit between podocyte foot proc
American Society for Clinical Investigation.
-
8. Neph1 and nephrin interaction in the slit diaphragm is an important determinant of glomerular permeability
Neph1-deficient mice develop nephrotic syndrome at birth, indicating the importance of this protein in the development of a normal glomerular filtration barrier. While the precise subcellular localization of Neph1 remains unknown, its relationship with other components of the glomerular filtration barrier is of great interest in this field. In this paper, we
American Society for Clinical Investigation.
-
9. Nephrin Deficiency Activates NF-κB and Promotes Glomerular Injury
Increasing evidence implicates activation of NF-κB in a variety of glomerular diseases, but the mechanisms involved are unknown. Here, upregulation of NF-κB in the podocytes of transgenic mice resulted in glomerulosclerosis and proteinuria. Absence of the podocyte protein nephrin resulted in NF-κB activation, suggesting that nephrin negatively regulates t
American Society of Nephrology.
-
10. Nck Proteins Maintain the Adult Glomerular Filtration Barrier
Within the glomerulus, the scaffolding protein nephrin bridges the actin-rich foot processes that extend from adjacent podocytes to form the slit diaphragm. Mutations affecting a number of slit diaphragm proteins, including nephrin, cause glomerular disease through rearrangement of the actin cytoskeleton and disruption of the filtration barrier. We recently
American Society of Nephrology.
-
11. Nephrin and CD2AP Associate with Phosphoinositide 3-OH Kinase and Stimulate AKT-Dependent Signaling
Mutations of NPHS1 or NPHS2, the genes encoding nephrin and podocin, as well as the targeted disruption of CD2-associated protein (CD2AP), lead to heavy proteinuria, suggesting that all three proteins are essential for the integrity of glomerular podocytes, the visceral glomerular epithelial cells of the kidney. It has been speculated that these proteins par
American Society for Microbiology.
-
12. Urine Podocyte mRNAs Mark Progression of Renal Disease
Because loss of podocytes associates with glomerulosclerosis, monitoring podocyte loss by measuring podocyte products in urine may be clinically useful. To determine whether a single episode of podocyte injury would cause persistent podocyte loss, we induced limited podocyte depletion using a diphtheria toxin receptor (hDTR) transgenic rat. We monitored podo
American Society of Nephrology.