IL-21 (human) (rec.) (His)
|Source/Host||HEK 293 cells|
|Sequence||Human IL-21 (aa 32-162) is fused at the C-terminus to a His-tag.|
|Biological Activity||Measured by a cell proliferation assay using human N1186 T cells. The ED50 for this effect is typically 10ng/mL, corresponding to a specific activity of 1x 105 units/mg|
|Endotoxin Content||<0.01EU/μg protein (LAL test; Lonza).|
Reconstitute 10µg vial with 100 µl sterile water to a concentration of 0.1mg/ml.
Reconstitute 50µg vial with 100 µl sterile water to a concentration of 0.5mg/ml.
Add 1X PBS to the desired protein concentration.
|Formulation||Lyophilized from 0.2μm-filtered solution in PBS.|
|Other Product Data||NCBI reference NP_068575.1: IL-21 (human)|
|Declaration||Manufactured by Chimerigen.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
Avoid freeze/thaw cycles.
Centrifuge lyophilized vial before opening and reconstitution.
PBS containing at least 0.1% BSA should be used for further dilutions.
Stable for at least 1 year after receipt when stored at -20°C.
Working aliquots are stable for up to 3 months when stored at -20°C.
|Product Specification Sheet|
Interleukin-21 (IL-21) is a key factor in the transition between innate and adaptive immune responses secreted by activated T cells. The IL-21 receptor (IL-21R) is expressed in lymphoid tissue, in particular by NK, B, T and dendritic cells, macrophages and endothelial cells. Recent evidence suggests that IL-21 plays a supportive role in the proliferation of T and B cells and influences the cytolytic activity of natural killer cells. IL-21 has been shown to up-regulate genes associated with innate immunity and to inhibit the differentiation of naïve T helper cells. IL-21 specifically inhibits IFN-γ production from developing TH1 cells and is preferentially expressed by TH2 cells. Furthermore IL-21 has been identified as a growth and survival factor for human myeloma cells. IL-21/IL-21R interactions have a unique role in sequentially activating both innate and adaptive immune responses against poorly immunogenic tumors, leading to tumor rejection that is perforin dependent but IFN-γ independent.