PROVETOP

Biotinylated Human CD94 Protein

Catalog No: CD94-HB001

Species
Human
Expression System
HEK293
Tag
His, Avi

Product overview

Recombinant Biotinylated Human CD94 Protein is expressed in HEK293 cells with a His tag and Avi tag at the N-terminus. It contains amino acid residues Ser34-Ile179 (UniProt accession: Q13241-1).

Product Details

Molecular Aliases
CD94; KLRD1; KP43; NK cell receptor
Protein Length
Ser34-Ile179
Expression System
HEK293
Theoretical Molecular Weight
The protein has a predicted MW of 19.8 kDa. Due to glycosylation, the protein migrates to 35-45 kDa based on Bis-Tris PAGE result.
Purity
> 95% as determined by Bis-Tris PAGE > 95% as determined by HPLC
Endotoxin
Less than 1 EU per μg by the LAL method.
Buffer / Formulation
Lyophilized from 0.22μm filtered solution in PBS (pH 7.4). Normally 8% trehalose is added as protectant before lyophilization.
State
Lyophilized
Storage Conditions
-20 to -80°C for 12 months as supplied from date of receipt. -80°C for 3 months after reconstitution. Recommend to aliquot the protein into smaller quantities for optimal storage. Please minimize freeze-thaw cycles.
Reconstitution Advice
Dissolve the lyophilized protein in distilled water. Please refer to the Certificate of Analysis for detailed instructions.

Data Display

Bis-Tris PAGE
CD94-HB001 Bis-Tris-PAGE-white result

Biotinylated Human CD94 on Bis-Tris PAGE under reduced conditions. The purity is greater than 95%.

SEC-HPLC
CD94-HB001 SEC-HPLC result

The purity of Biotinylated Human CD94 is greater than 95% as determined by SEC-HPLC.

Background

CD94 is an approximately 25 kDa type 2 transmembrane protein that plays an important role in regulating natural killer (NK) cell activation. CD94 plays a role as a receptor for the recognition of MHC class I HLA-E molecules by NK cells and some cytotoxic T-cells.

References

  1. Walsh C E, Ryan E J, Cliona O'Farrelly, et al. Differential Expression of NK Receptors CD94 and NKG2A by T Cells in Rheumatoid Arthritis Patients in Remission Compared to Active Disease[J]. PLOS ONE, 2011, 6.

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