Recombinant Human PILR-beta Fc Chimera Protein, CF

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When Recombinant Human CL‑P1/COLEC12 (Catalog # 2690‑CL) is coated at 2 μg/mL, Recombinant Human PILR‑beta Fc Chimera(Catalog # 9828‑PR) binds with an ED50 of 0.12‑0.72 μg/mL.

Product Details

Summary
Reactivity HuSpecies Glossary
Applications Bioactivity
Format
Carrier-Free

Order Details

Recombinant Human PILR-beta Fc Chimera Protein, CF Summary

Details of Functionality
Measured by its binding ability in a functional ELISA. Recombinant Human CL-P1/COLEC12 (Catalog # 2690-CL) immobilized at 2 μg/mL, 100 μg/mL, can bind to Recombinant Human PILR‑ beta Fc Chimera with an ED50 of 0.12-0.72 μg/mL.
Source
Human embryonic kidney cell, HEK293-derived human PILR-beta protein
Human PILR-beta
(Gln20-Ala189)
Accession # Q9UKJ0-1
IEGRMD Human IgG1
(Pro100-Lys330)
N-terminusC-terminus
Accession #
N-terminal Sequence
No results obtained. Gln20 predicted.
Structure / Form
Disulfide-linked homodimer
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
45.7 kDa (monomer).
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
57-66 kDa, 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-beta Fc Chimera Protein, CF

  • activating receptor PILRbeta
  • Activating receptor PILR-beta
  • Cell surface receptor FDFACT
  • cell surface receptor FDFACT1
  • cell surface receptor FDFACT2
  • FDFACT
  • FDFACT1
  • FDFACT2
  • paired immunoglobin-like receptor beta
  • paired immunoglobin-like type 2 receptor beta
  • paired immunoglobulin-like receptor beta
  • paired immunoglobulin-like type 2 receptor beta
  • PILRB
  • PILRbeta
  • PILR-beta

Background

Paired immunoglobulin-like type 2 receptor beta (PILR-beta ) is a type I transmembrane (TM) glycoprotein belonging to the Ig superfamily. PILR-beta is the activating counterpart to the immunoreceptor tyrosine-based inhibitory motif (ITIM) containing PILR-alpha inhibitory receptor (1). Mature human PILR-beta is a 208 amino acid (aa) protein containing a 172 aa V-type Ig-like extracellular domain (ECD) with a siglec-like fold, a single TM, and a truncated cytoplasmic tail (2, 3). The TM of PILR-beta contains a positively-charged residue which interacts with immunoreceptor tyrosine-based activation (ITAM)-bearing adaptor molecules (2). The ECD of mature human PILR-beta shares 40% aa sequence identity with its mouse counterpart. PILR-beta is expressed on myeloid cells, such as natural killer, macrophage, and dendritic cells, as well as resident cells of the central nervous system, such as microglial cells (2,4). It is a binding partner for DAP12 and CD99, and has been shown to play an important role in innate immunity and inflammation (4-6). The PILR-alpha / beta pair have also been shown to regulate cell signaling via association with SHP-1 (7). Experiments studying the effects of S. aureus and T. gondii infections in mice have shown that up-regulation of PILR-beta led to significantly lower survival rates while knock-down of PILR-beta or activation of PILR-alpha resulted in significantly less inflammation and increased pathogen clearance (4,5).

  1. Wilson, M.D. et al. (2006) Physiol. Genomics 27:201.
  2. Shiratori, I. et al. (2004) J. Exp. Med. 199:525.
  3. Lu, Q. et al. (2014) PNAS 111:8221.
  4. Tato, C.M. et al. (2012) PLoS One 7:e31690.
  5. Banerjee, A. et al. (2010) Infect. Immun. 78:1353.
  6. Tabata, S. et al. (2008) J. Biol. Chem. 283:8893.
  7. Mousseau, DD. et al. (2000) J. Biol. Chem. 275:4467.

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