MABS455
Anti-GLEPP1 Antibody, extracellular domain, clone 1B4
clone 1B4, 1 mg/mL, from mouse
Synonym(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
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
antibody form
purified antibody
antibody product type
primary antibodies
clone
1B4, monoclonal
species reactivity
rat
concentration
1 mg/mL
technique(s)
immunohistochemistry: suitable
western blot: suitable
isotype
IgG2aκ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
rat ... Ptpro(50677)
General description
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.
Immunogen
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).
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.
Quality
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.
Immunohistochemistry Analysis: A 1:50-250 dilution of this antibody detected GLEPP1, extracellular domain in glomeruli of rat kidney tissue.
Target description
138 kDa calculated
Physical form
Format: Purified
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Storage Class
12 - Non Combustible Liquids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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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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