Recombinant Human PILR-alpha Fc Chimera Protein, CF

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2 μg/lane of Recombinant Human PILR-alpha Fc Chimera (Catalog # 10802-PR) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at ...read more

Product Details

Summary
Reactivity HuSpecies Glossary
Applications Bioactivity
Format
Carrier-Free

Order Details

Recombinant Human PILR-alpha Fc Chimera Protein, CF Summary

Details of Functionality
Measured by its binding ability in a functional ELISA. When Recombinant Human PANP Fc Chimera (Catalog # 7920-PN) is coated at 5.00 µg/mL (100 μL/well), Recombinant Human PILR- alpha Fc Chimera binds with an ED50 of 0.150- 0.900 μg/mL.
Source
Chinese Hamster Ovary cell line, CHO-derived human PILR-alpha protein
Human PILR-alpha
(Thr25-Thr196)
Accession # Q9UKJ1.3
IEGRMD Human IgG1
(Pro100-Lys330)
N-terminusC-terminus
Accession #
N-terminal Sequence
Thr25
Protein/Peptide Type
Recombinant Proteins
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.

Applications/Dilutions

Dilutions
  • Bioactivity
Theoretical MW
46 kDa.
Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
57-64 kDa, under reducing conditions

Packaging, Storage & Formulations

Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose.
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining
Reconstitution Instructions
Reconstitute at 500 μg/mL in PBS.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Recombinant Human PILR-alpha Fc Chimera Protein, CF

  • Cell surface receptor FDF03
  • FDF03
  • inhibitory receptor PILRalpha
  • Inhibitory receptor PILR-alpha
  • paired immunoglobin-like receptor alpha
  • paired immunoglobin-like type 2 receptor alpha
  • paired immunoglobulin-like receptor alpha
  • paired immunoglobulin-like type 2 receptor alpha
  • PILRA
  • PILRalpha
  • PILR-alpha

Background

Paired immunoglobulin-like type 2 receptor-alpha (PILRA) is one of two members that belong to a small family of immunoregulatory Ig-superfamily receptors (1-4). It is a counterpart to PILRB and the PILRs represent one of many pairs of Ig-like domain-containing receptors that participate in immune regulation (1, 2). Mature human PILRA consists of an extracellular domain (ECD) with one V-type Ig-like domain, a transmembrane domain, and a cytoplasmic domain with two immunoreceptor Tyr‑based inhibitory (ITIM) motifs. Given that ITIMs are known to interact with phosphatases such as PTPN6 and PTPN11, the presence of these motifs makes PILRA an inhibitory receptor (1-4). The ECD of human PILRA shares 42% and 40% amino acid sequence identity with mouse and rat PILRA, respectively. Three potential isoforms for human PILRA have been reported. PILRA is expressed by neutrophils, macrophages, monocytes, mast cells, APCs, microglia, neurons, cardiac muscle and renal proximal plus pancreatic duct eipthelium (4, 7, 8). It has multiple binding partners, including CD99 (4, 9), glycoprotein B/gB of HSV1 (in human) (7), PANP (PILR-associated neural protein) (8) and NPDC1 plus collectin-12 (10). Although PILRA and PILRB are highly similar in their ECD amino acid sequence, they do not necessarily share the same ligands, as PILRB fails to bind to gB and PANP (8, 10). PILRA binding appears to be dependent upon the presence of a poorly-defined peptide sequence coupled to a sialylated, O-linked carbohydrate motif but its exact function remains unclear (5, 9-12). Up-regulation of PILRA in the early stage of immune reaction and its subsequent binding to CD99 may lead to a down-regulation of the inflammatory response (10). Genome-wide association studies (GWAS) have linked PILRA to Alzheimer's Disease (AD) through association of PILRB with ZCWPW1 (13,14). It was further supported that ZCWPW1 locus SNP rs1476679 was associated with reduced PILRA levels suggesting a potential role for the gene in AD (15). The missense variant (G78R, rs1859788) of PILRA is thought to be the causal allele for the confirmed AD risk locus. The variant reduced the binding of PILRA to several ligands including a novel ligand, complement component 4A, and herpes simplex virus 1 (HSV-1) glycoprotein B (16). The observed protection from AD risk by PILRA G78R variant provided a new candidate for the therapeutic target.
  1. Wilson, M.D. et al. (2006) Physiol. Genomics 27:201.
  2. Lanier, L.L. (2001) Curr. Opin. Immunol. 13:326.
  3. Fournier, N. et al. (2000) J. Immunol. 165:1197.
  4. Shiratori, I. et al. (2004) J. Exp. Med. 199:525.
  5. Mousseau, D.D. et al. (2000) J. Biol. Chem. 275:4467.
  6. SwissProt Accession # Q9UKJ1.
  7. Tato, C.M. et al. (2012) PLoS ONE 7:e31680.
  8. Satoh, T. et al. (2008) Cell 132:935.
  9. Tabata, S. et al. (2008),J. Biol. Chem. 283:8893.
  10. Sun, Y. et al. (2012) J. Biol. Chem. 287:15837.
  11. Wang, J. et al. (2008) J. Biol. Chem. 180:1686.
  12. Arii, J. et al. (2010) J. Virol. 84:10733.
  13. Karch, CM. et al. (2016) PLoS ONE. 11:1-22.
  14. Allen, M. et al. (2015) Neurol Genet. 1:e15 (PubMed: 27066552).
  15. Patel, T. et al. (2018) Neurolpathol Appl Neurobiol. 44(5):506.
  16. Rathore, N. et al. (2018) PLoS Genet. 14(11):e1007427.

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