The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Measured by its binding ability in a functional ELISA. Immobilized rhIL7Ra Fc Chimera at 0.25 μg/ml ( 100 μl/well ) on a Rabbit anti-human IgG Fc antibody, the concentration of rhIL7 that produces 50% of the optimal binding response is found to be approximately 20 - 100 ng/mL
< 1.000 Eu/µg
>95% by SDS-PAGE .
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Store at 4°C prior to reconstitution. Upon reconsitution add a carrier protein (0.1% BSA). Store at -20°C or -80°C. Avoid freeze / thaw cycle.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
It is recommended to reconstitute the lyophilized product in 1000 µl sterile deionized water to a final concentration of 1 mg/ml. Solubilize for 30 to 60 minutes at room temperature with occasional gentle mixing. Carrier protein (0.1% HSA or BSA) is strongly recommended for further dilution and long term storage
IL 7R alpha
IL-7 receptor subunit alpha
IL-7R subunit alpha
Interleukin 7 receptor
Interleukin 7 receptor alpha chain
Interleukin 7 receptor isoform H5 6
Interleukin-7 receptor subunit alpha
Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP).
Involvement in disease
Defects in IL7R are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:608971]. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development. Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3) [MIM:612595]. A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheat, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=A polymorphism at position 244 strongly influences susceptibility to multiple sclerosis. Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele (Thr-244) or 'T' allele (Ile-244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.
Belongs to the type I cytokine receptor family. Type 4 subfamily. Contains 1 fibronectin type-III domain.
The WSXWS motif appears to be necessary for proper protein folding and thereby efficient intracellular transport and cell-surface receptor binding. The box 1 motif is required for JAK interaction and/or activation.
N-glycosylated IL-7Ralpha binds IL7 300-fold more tightly than the unglycosylated form.