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#29070 Anti-Human Nephrin (C) Rabbit IgG Affinity Purify

  • WB_IP
  • rat renal glomerular lysate (7.5% gel)
  • Rat renal glomerular (FITC)
  • Human renal glomerular (DAB)
Intended Use:
Research reagents
Application:
WB, IP, IHC
Package Size1:
100 μg
Package Size2:
10 μg
Note on Application Abbreviations
WB:Western Blotting
IP:Immunoprecipitation
IHC:Immunohistochemistry

※ The product indicated as "Research reagents" in the column Intended Use cannot be used
  for diagnostic nor any medical purpose.
※ The datasheet listed on this page is sample only. Please refer to the datasheet
  enclosed in the product purchased before use.

Product Overview

Product Overview

Product Code 29070
Product Name Anti-Human Nephrin (C) Rabbit IgG Affinity Purify
Intended Use Research reagents
Application WB, IP, IHC
Species Human
Immunizing antigen Synthetic peptide of the C-terminal part of Human Nephrin
Purification Method Purified with antigen peptide
Specificity Cross-reacts with rat.
Package Form Lyophilized product from 1% BSA in PBS containing 0.05% NaN3
Storage Condition 2 - 8℃
Poisonous and Deleterious Substances Applicable
Cartagena Not Applicable
Package Size 1 100 μg
Package Size 2 10 μg
Remarks1 The commercial use of products without our permission is prohibited. Please make sure to contact us and obtain permission.

Product Description

Product Description

The kidney is an important organ that maintains a homeostasis of body-fluid and nutrition. The capillary walls of renal glomeruli allow the efficient removal of the metabolic waste (filter) and conservation of essential circulating proteins, such as albumin (barrier). The filtration barriers are composed of three layers: a fenestrated endothelium, the glomerular basement membrane, and the highly specialized epithelial cells, podocytes. The podocytes elaborate numerous cellular processes and the terminal portions, called foot process, cover the outmost surface of the glomerular basement membrane. The neighboring foot processes are aligned in an interdigitating fashion while leaving a filtration slit around 20-50nm in wide that is bridged by an electron dense membrane-like structure, the slit diaphragm. Recent studies with familial nephrotic syndrome and genetically manipulated mice models demonstrated the genetic defects of the slit diaphragm proteins (nephrin, podocin, etc) cause massive proteinuria (nephrotic syndrome) and eventually progress the end stage renal diseases. The observations indicate that regulation of the slit diaphragm integrity is crucial for maintenance of the filtration barrier function and podocyte viability. Nephrin has been identified as a disease causing molecule responsible for congenital nephrotic syndrome of Finnish type, in which the proteinuria starts in utero or immediately after birth. It is an immunoglobulin-like transmembrane adhesion protein having eight Ig motifs. Nephrin forms a structural backbone of the slit diaphragm through a head-to-head, trans-homo-interaction at the N-terminal ectodomains. In addition to the structural function, nephrin serves as a signaling molecule that mediate an adaptive morphological regulation through the remodeling of actin cytoskeletons; the C-terminal cytoplasmic domain is tyrosine-phosphorylated by Src family kinase (Fyn) and the phosphorylated nephrin associates with an SH2 adaptor protein (Nck), thereby allowing the sable anchorage of the slit membrane complex to the actin cytoskeleton in the foot processes. Under proteinuric conditions, nephrin is down-regulated and is apically dislocated.

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