Mouse IL-4 R alpha / CD124 Protein, His Tag

Source : 

Mouse IL-4 R alpha, His Tag (ILR-M52H1) is expressed from human 293 cells (HEK293). It contains AA Ile 26 - Arg 233 (Accession # NP_001008700).

 

Molecule : IL-4 R alpha

 

Synonyms : IL4R,CD124,IL4RA

 

Format : Powder

 

Category : Bio-Markers & CD Antigens

 

Accession : NP_001008700

 

Storage : -20℃

 

Shipping condition : Powder,RT

 

Molecular Weight : 26.3 kDa

 

Characteristics :

This protein carries a polyhistidine tag at the C-terminus. The protein has a calculated MW of 26.3 kDa. The protein migrates as 37-45 kDa under reducing (R) condition (SDS-PAGE).

 

Endotoxin Level : Less than 1.0 EU per μg by the LAL method.

 

Buffer : PBS, pH7.4

 

Description :

IL-4 is a pleiotropic cytokine produced by activated Th2 cells and mast cells, and plays a pivotal role in immune responses. The effects of IL-4 are mediated after binding to high affinity receptor complexes present on hematopoietic as well as non-hematopoietic cells. Hematopoietic cellular responses to IL-4 are mediated by a high affinity receptor complex comprised of the 140 kDa IL4Rα (CD124)subunit and the 70 kDa common cytokine γc chain (CD132).
Interleukin 4 Receptor (IL4R) also known as CD124, IL4Rα and BSF receptor, is a type I cytokine receptor produced by activated Th2 cells and mast cells, and plays an important role in Th2-­biased immune responses, alternative macrophage activation, mucosal immunity, allergic inflammation, tumor progression, and atherogenesis. A soluble form of the encoded IL4R protein can be produced by an alternate splice variant or by proteolysis of the membrane-bound protein, and this soluble form can inhibit IL4-mediated cell proliferation and IL5 upregulation by T-cells. IL4R can alternatively associate with IL­13Ra1 to form the type II receptor which is responsive to both IL­4 and IL­13. Interleukin-4 receptor has been shown to interact with SHC1.

 

References :

(1) Ikizawa, K., et al., 2000, Biochem. Biophys. Res. Commun. (UNITED STATES) 268 (1): 54–9.
(2) Kashiwada, M., et al., 2001, J. Immunol. (United States) 167 (11): 6382–7.
(3) Hage T., et al., 1999, Cell 97 (2): 271–81.
(4) Gessner,A. et al., 2000, Immunobiology. 201 (3-4): 285-307.
(5) Wills­Karp, M., F.D. Finkelman, 2008, Sci. Signal. 1:pe55.