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MABS1221

Sigma-Aldrich

Anti-GLEPP1/PTPRO Antibody, clone 5C11

clone 5C11, from mouse

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Synonym(s):
Receptor-type tyrosine-protein phosphatase O, Glomerular epithelial protein 1, Osteoclastic transmembrane protein-tyrosine phosphatase, Protein tyrosine phosphatase U2, PTP-OC, PTP phi, PTP-U2, PTPase U2, R-PTP-O
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

5C11, monoclonal

species reactivity

human

should not react with

mouse, rat, rabbit

technique(s)

electron microscopy: suitable
immunofluorescence: suitable
immunohistochemistry: suitable

isotype

IgG2bκ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... PTPRO(5800)

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antibody form

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purified immunoglobulin

antibody form

purified immunoglobulin

antibody form

purified antibody

clone

5C11, monoclonal

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3F4, monoclonal

clone

FG6-1G, monoclonal

clone

scFvs 45, monoclonal

species reactivity

human

species reactivity

human

species reactivity

human

species reactivity

human

technique(s)

electron microscopy: suitable, immunofluorescence: suitable, immunohistochemistry: suitable

technique(s)

indirect ELISA: suitable, western blot: 1-5 μg/mL

technique(s)

immunoprecipitation (IP): suitable, western blot: suitable

technique(s)

immunoprecipitation (IP): suitable

isotype

IgG2bκ

isotype

IgG2aκ

isotype

IgG2aκ

isotype

-

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General description

Receptor-type tyrosine-protein phosphatase O (EC 3.1.3.48; UniProt Q16827; also known as Glomerular epithelial protein 1, Osteoclastic transmembrane protein-tyrosine phosphatase, Protein tyrosine phosphatase U2, PTP-OC, PTP phi, PTP-U2, PTPase U2, R-PTP-O) is encoded by the PTPRO (also known as GLEPP1, NPHS6, PTPROT, PTPU2) gene (Gene ID 5800) in human. Podocytes are complex neuron-like post-mitotic cells adherent to the underlying glomerular basement membrane via foot processes that must contiguously cover the filtration surface area to maintain the normal filtration barrier. Glomerular epithelial protein 1 (GLEPP1) is a podocyte receptor membrane protein tyrosine phosphatase located on the apical cell membrane of visceral glomerular epithelial cell (VGEC) foot processes and is commonly used as a podocyte marker for assessing podocyte density. Altered GLEPP1 staining patterns are reported in kidney sections from individuals with congenital nephrotic syndrome of the Finnish type (CNF), minimal-change nephropathy (MCN), and Hodgkin’s disease. GLEPP1 is initially produced with a signal peptide sequence (a.a. 1-29), the removal of which yields the mature protein with a large extracellular region (a.a. 30-822), followed by a transmembrane segment (a.a. 823-843) and a cytoplasmic domain (a.a. 844-1216).

Specificity

Clone 5C11 recognizes GLEPP1 (PTPRO) in human podocytes and neurons, but not GLEPP1 spliced isoforms lacking Fibronectin type-III domains 1-5 in their extracellular region in many other cells. Clone 5C11 detected a 200 kD protein band in glomerular extracts by Western blotting under both reducing and nonreducing conditions and immunostained only visceral glomerular epithelial cell (VGEC) in human renal cortex tissues by both fluorescent and non-fluorescent immunohistochemistry (Sharif, K., et al. (1998). Exp. Nephrol. 6(3):234-244).

Immunogen

Epitope: Fibronectin type-III domains 1-5.
GST-tagged recombinant fragment corresponding to the Fibronectin type-III domains 1-5 of human GLEPP1/PTPRO.

Application

Detect GLEPP1/PTPRO using this Anti-GLEPP1/PTPRO Antibody, clone 5C11 validated for use in Immunohistochemistry, Immunofluorescence, Electron Microscopy.
Immunohistochemistry Analysis: A representative lot detected a loss of GLEPP1 immunoreactivity as a measure of podocyte density reduction (podocyte depletion) in kidney tissues with transplant glomerulopathy using formalin-fixed, paraffin-embedded kidney sections (Yang, Y., et al. (2015). J. Am. Soc. Nephrol. 26(6):1450-1465).
Immunofluorescence Analysis: Prior to purification, clone 5C11 hybridoma culture supernatant detected GLEPP1 (PTPRO) immunoreactivity predominantly on visceral glomerular epithelial cell (VGEC) foot processes along the glomerulus (GBM) in manthanol-fixed, adult human kidney cryosections, while altered GLEPP1 staining patterns were seen in kidney sections from individuals with congenital nephrotic syndrome of the Finnish type (CNF), minimal-change nephropathy (MCN), or Hodgkin’s disease (Sharif, K., et al. (1998). Exp. Nephrol. 6(3):234-244).
Electron Microscopy Analysis: Prior to purification, clone 5C11 hybridoma culture supernatant detected GLEPP1 (PTPRO) immunoreactivity at the apical aspect of the foot processes and the cell membrane of larger processes in paraformaldehyde-fixed, paraffin-embedded normal human adult kidney sections, while GLEPP1 immunoreactivity was seen redistributed from glomerulus (GBM) on the apical cell membrane of VGECs to microvilli on kidney sections from individuals with congenital nephrotic syndrome of the Finnish type (CNF) or minimal-change nephropathy (MCN) (Sharif, K., et al. (1998). Exp. Nephrol. 6(3):234-244).

Quality

Evaluated by Immunohistochemistry in human kidney tissue.

Immunohistochemistry Analysis: A 1:50 dilution of this antibody detected GLEPP1/PTPRO in human kidney tissue.

Target description

200 kDa calculated.

Physical form

Format: Purified

Other Notes

Concentration: Please refer to lot specific datasheet.

Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Kathryn E Haley et al.
Frontiers in physiology, 12, 625762-625762 (2021-08-03)
Podocyte loss plays a pivotal role in the pathogenesis of glomerular disease. However, the mechanisms underlying podocyte damage and loss remain poorly understood. Although detachment of viable cells has been documented in experimental Diabetic Nephropathy, correlations between reduced podocyte density
Sergi Clotet-Freixas et al.
Journal of the American Society of Nephrology : JASN, 31(11), 2705-2724 (2020-09-10)
Antibody-mediated rejection (AMR) accounts for >50% of kidney allograft loss. Donor-specific antibodies (DSA) against HLA and non-HLA antigens in the glomeruli and the tubulointerstitium cause AMR while inflammatory cytokines such as TNFα trigger graft injury. The mechanisms governing cell-specific injury

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