Recombinant Human PILR-alpha Fc Chimera Avi-tag Protein, CF Summary
Additional Information |
Biotinylated |
Details of Functionality |
The biotin to protein ratio is greater than 0.7 as determined by the HABA assay. Measured by its binding ability in a functional ELISA. When Recombinant Human PANP Fc Chimera
(Catalog #
7920-PN)
is coated at 5 μg/mL, 100 μL/well, Biotinylated Recombinant Human PILR‑ alpha Fc Chimera Avi-tag (Catalog # AVI10702) binds with an ED 50 of 0.6-6 μg/mL. |
Source |
Chinese Hamster Ovary cell line, CHO-derived human PILR-alpha protein Human PILR-alpha (Gln20-Thr196) Accession # Q9UKJ1.3 | IEGRMD | Human IgG1 (Pro100-Lys330) | Avi-tag | N-terminus | | | C-terminus | |
|
Accession # |
|
N-terminal Sequence |
Thr25 |
Structure / Form |
Disulfide-linked homodimer, biotinylated via Avi-tag |
Protein/Peptide Type |
Recombinant Proteins |
Purity |
>90%, 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 |
48 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 |
60-70 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, -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after opening.
- 3 months, -20 to -70 °C under sterile conditions after opening.
|
Buffer |
Supplied as a 0.2 μm filtered solution in PBS. |
Purity |
>90%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining. |
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 Avi-tag 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 downregulation 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 therapeutic target. Our Avi-tag Biotinylated human PILRA Fc Chimera features biotinylation at a single site contained within the Avi-tag, a unique 15 amino acid peptide. Protein orientation will be uniform when bound to streptavidin-coated surface due to the control of biotinylation and the rest of the protein is unchanged so there is no interference in the protein's bioactivity.
- 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):506-521.
- Rathore, N. et al. (2018) PLoS Genet. 14(11):e1007427.
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