IL-4R alpha/CD124 Protein, Mouse (233a.a, HEK293, Fc)

IL-4R alpha is a subunit alpha shared by IL-4 and IL-13 receptors, found in leukocytes originally. IL-4R alpha couples to the JAK1/2/3-STAT6 pathway and involves in promoting Th2 differentiation. IL-4R alpha/CD124, Mouse consists of 810 amino acids (M1-S810), exerts IL-4 binding function and results the phosphorylation of C-terminal tyrosine residues. IL-4R alpha/CD124, Mouse has an immunoreceptor tyrosine inhibitor motif (ITIM) (707-712 a.a), which can bind to the SH2 domain of some phosphatases by phosphorylating ITIM. IL-4R alpha/CD124, Mouse has a transmembrane domain (234-257 a.a). IL-4R alpha/CD124 Protein, Mouse (R1-R233) is produced in HEK293 cells, including a Fibronectin typr III domain (126-224 a.a) and a C-terminal hFC-tag.

Interleukin-4R alpha (IL-4Rα), also known as CD124 and B cell stimulatory factor (BSF) receptor, is one of the anti-inflammatory cytokines, and highly expressed in activated T-cells^[1].
IL-4R alpha participates in forming two interleukin receptors in different cell types. For the type I receptor, depends on IL-4R alpha binding IL-4 to recruit IL-2R gamma chain in immune cells. IL-2R gamma is the common subunit for a variety of interleukin receptors, involved in the stimulation of neutrophil phagocytosis by IL-15. For the type II receptor, depends on IL-4R alpha binding IL-4 to recruit IL-13R alpha 1 chain. IL-13R alpha 1 is an alternat accessory protein to the common cytokine receptor gamma chain in non-immune cells^[2][3].
The sequence of amino acids in IL-4R alpha proteins in mouse shows low homology with human (52.82%) and rat (53.35%).
需要补上 IL-4 R alpha generates a soluble form by alternate splicing or proteolysis, maintaining ligand binding properties and inhibiting IL-4 bioactivity. IL-4 R alpha soluble isoform 1 can be produced by proteolytic cleavage at the cell surface (shedding) by a metalloproteinase^[4].
IL-4 R alpha plays an important role in Th2-biased immune responses, alternative macrophage activation, mucosal immunity, allergic inflammation, tumor progression, and atherogenesis^[5].

IL-4 R alpha plays a key role in the control of RSV-induced lung injury by alternatively activated macrophages, and induces AA-Mφ differentiation^[6].
IL-4 R alpha deficiency, in IL-4R alpha^-/- RSV infected mice model, leads to strong inflammation in the lungs compared with control^[6].

IL-4 R alpha is regulated by IFN-beta in response to RSV (severe respiratory syncytial virus), exhibits sustained proinflammatory cytokine production^[6].

Mouse

HEK293

C-hFc

Q3U905 (M1-R233)

16190  [NCBI]

Approximately 51.1 kDa

Greater than 95% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.

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