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Principaux documents

MABS455

Sigma-Aldrich

Anti-GLEPP1 Antibody, extracellular domain, clone 1B4

clone 1B4, 1 mg/mL, from mouse

Synonyme(s) :

Receptor-type tyrosine-protein phosphatase O, R-PTP-O, Glomerular epithelial protein 1, Protein tyrosine phosphatase U2, PTP-U2, PTPase U2, Ptpro

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

mouse

Forme d'anticorps

purified antibody

Type de produit anticorps

primary antibodies

Clone

1B4, monoclonal

Espèces réactives

rat

Concentration

1 mg/mL

Technique(s)

immunohistochemistry: suitable
western blot: suitable

Isotype

IgG2aκ

Numéro d'accès NCBI

NP_059032

Numéro d'accès UniProt

Q62797

Conditions d'expédition

wet ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

rat ... Ptpro(50677)

Description générale

YGlomerular epithelial protein 1 (GLEPP1) is a membrane bound tyrosine phosphatase present on the apical cell surface that plays a role in regulating the glomerular pressure filtration rate by regulating podocyte structure and function. GLEPP1 is expressed in the kidney but also in brain, lung and placenta. In the brain, GLEPP1 plays an important role in axon guidance, and in other cells GLEPP1 assists in lamellipodium assembly. Because of its action on lamellipodia, GLEPP1 is important in cellular chemotaxis, thus inhibitors to GLEPP1 function aid in treatments where the migration of inflammatory cells are affected such as in ulcerative colitis. Finally, because phosphorylation and its reversal via phosphatases are key signaling and regulatory events, a variety of syndromes are associated with genetic variations associated with phosphatase mutations. For GLEPP1, various nephrotic syndromes such as NPHS6 and hyper-proteinuria disease are associated with mutations in the GLEPP1 coding region.

Immunogène

Recombinant protein corresponding to rat GLEPP1, extracellular domain.

Application

Immunohistochemistry Analysis: A representative lot detected GLEPP1, extracellular domain in isolated rat glomeruli tissue (Wharram, B.L., et al. (2005) J Am Soc Nephrol. 16:2941–2952; Fukuda, A., et al. (2012). Kidney International. 81:40-55; Kim, Y.H., (2001). Kidney International. 60:957-968).
Western Blotting Analysis: A representative lot detected GLEPP1, extracellular domain in rat isolated glomeruli tissue lysate (Fukuda, A., et al. (2012). J Am Soc Nephrol. 23:1351–1363).
This Anti-GLEPP1 Antibody, extracellular domain, clone 1B4 is validated for use in Immunohistochemistry and Western Blotting for the detection of GLEPP1, extracellular domain.

Qualité

Evaluated by Immunohistochemistry in glomeruli of rat kidney tissue.

Immunohistochemistry Analysis: A 1:50-250 dilution of this antibody detected GLEPP1, extracellular domain in glomeruli of rat kidney tissue.

Description de la cible

138 kDa calculated

Forme physique

Format: Purified

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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Angiotensin II-dependent persistent podocyte loss from destabilized glomeruli causes progression of end stage kidney disease.
Fukuda, Akihiro, et al.
Kidney International, 81, 40-55 (2012)
Podocyte depletion and glomerulosclerosis have a direct relationship in the PAN-treated rat.
Kim, Y H, et al.
Kidney International, 60, 957-968 (2001)
Podocyte depletion causes glomerulosclerosis: diphtheria toxin-induced podocyte depletion in rats expressing human diphtheria toxin receptor transgene.
Wharram, Bryan L, et al.
Journal of the American Society of Nephrology, 16, 2941-2952 (2005)
Akihiro Fukuda et al.
Journal of the American Society of Nephrology : JASN, 23(8), 1351-1363 (2012-07-10)
Podocyte depletion leads to glomerulosclerosis, but whether an impaired capacity of podocytes to respond to hypertrophic stress also causes glomerulosclerosis is unknown. We generated transgenic Fischer 344 rats that express a dominant negative AA-4E-BP1 transgene driven by the podocin promoter;

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