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 ED 50 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-terminus | | C-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 |
|
| 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
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.
- Wilson, M.D. et al. (2006) Physiol. Genomics 27:201.
- Lanier, L.L. (2001) Curr. Opin. Immunol. 13:326.
- Fournier, N. et al. (2000) J. Immunol. 165:1197.
- Shiratori, I. et al. (2004) J. Exp. Med. 199:525.
- Mousseau, D.D. et al. (2000) J. Biol. Chem. 275:4467.
- SwissProt Accession # Q9UKJ1.
- Tato, C.M. et al. (2012) PLoS ONE 7:e31680.
- Satoh, T. et al. (2008) Cell 132:935.
- Tabata, S. et al. (2008),J. Biol. Chem. 283:8893.
- Sun, Y. et al. (2012) J. Biol. Chem. 287:15837.
- Wang, J. et al. (2008) J. Biol. Chem. 180:1686.
- Arii, J. et al. (2010) J. Virol. 84:10733.
- Karch, CM. et al. (2016) PLoS ONE. 11:1-22.
- Allen, M. et al. (2015) Neurol Genet. 1:e15 (PubMed: 27066552).
- Patel, T. et al. (2018) Neurolpathol Appl Neurobiol. 44(5):506.
- Rathore, N. et al. (2018) PLoS Genet. 14(11):e1007427.
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