Recombinant Human PILR-beta His-tag Protein, CF Summary
Gln20-Ala189, with a C-terminal 6-His tag
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CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
|Formulation||Supplied as a 0.2 μm filtered solution in PBS.|
|Shipping||The product is shipped with dry ice or equivalent. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
2 μg/lane of Recombinant Human PILR-beta His-tag Protein (Catalog # 10319-PR) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing a band at 30-40 kDa under reducing and non-reducing conditions.
Paired immunoglobulin-like type 2 receptor beta (PILR-beta ) is a type I transmembrane (TM) glycoprotein that belongs to the Ig superfamily (1). PILR-beta is the activating counterpart to the inhibitory receptor immunoreceptor PILR-alpha which contains a tyrosine-based inhibitory motif (ITIM) (1). Mature human PILR-beta contains a V‑type Ig‑like extracellular domain (ECD) with a siglec-like fold, a single TM domain, and a truncated cytoplasmic tail (2, 3). The TM domain 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% amino acid 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, including 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).
- Wilson, M.D. et al. (2006) Physiol. Genomics 27:201.
- Shiratori, I. et al. (2004) J. Exp. Med. 199:525.
- Lu, Q. et al. (2014) PNAS 111:8221.
- Tato, C.M. et al. (2012) PLoS One 7:e31690.
- Banerjee, A. et al. (2010) Infect. Immun. 78:1353.
- Tabata, S. et al. (2008) J. Biol. Chem. 283:8893.
- Mousseau, D.D. et al. (2000) J. Biol. Chem. 275:4467.
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