IFN-beta Protein, Human (CHO)

IFN-β (interferon-β) is a key type I interferon cytokine that coordinates the innate immune response to infection, tumors, and inflammation. IFN-β binds to high-affinity (IFNAR2) and low-affinity (IFNAR1) heterodimeric receptors, activates Jak-STAT signaling, and modulates interferon-regulated genes. IFN-beta Protein, Human (CHO) is the recombinant human-derived IFN-beta protein, expressed by CHO , with tag free.

IFN-beta (Interferon-beta), a pivotal type I interferon cytokine, assumes a critical role in orchestrating the innate immune response to various challenges, including infections, tumor development, and inflammatory stimuli. Acting through a high-affinity (IFNAR2) and low-affinity (IFNAR1) heterodimeric receptor, IFN-beta triggers the canonical Jak-STAT signaling pathway, leading to the transcriptional activation or repression of interferon-regulated genes. These genes, in turn, encode effectors crucial for the interferon response, encompassing antiviral proteins, regulators of cell proliferation and differentiation, and immunoregulatory proteins. While primarily signaling through the IFNAR1-IFNAR2 heterodimeric receptor, IFN-beta also demonstrates versatility by functioning with IFNAR1 alone and operating independently of Jak-STAT pathways. Its multifaceted effects span antiviral and antibacterial activities, modulation of B-cell development, myelopoiesis, and lipopolysaccharide-inducible production of tumor necrosis factor. In the realm of neuronal homeostasis, IFN-beta emerges as a guardian, regulating dopamine turnover and safeguarding dopaminergic neurons through the promotion of neuronal autophagy and alpha-synuclein clearance, thereby averting dopaminergic neuron loss. Notably, IFN-beta surpasses interferon-alpha (IFN-alpha) in potency, particularly in inducing apoptotic and antiproliferative pathways crucial for controlling tumor cell growth. Presenting as a monomer, IFN-beta embodies a versatile and potent player in diverse physiological responses and immune regulation.

1.Measured in antiviral assays using WISH cells infected with vesicular stomatitis virus and the ED₅₀ is 1-20 pg/mL.
2.Determined by a cytotoxicity assay using human TF-1 cells. The ED₅₀ for this effect is 0.07167 ng/mL, corresponding to a specific activity of 1.395 x 10⁷ units/mg.

Human

CHO

Tag Free

P01574 (M22-N187)

3456  [NCBI]

MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN

Approximately 20-23 kDa due to the glycosylation.

Greater than 95% as determined by reducing SDS-PAGE

Lyophilized powder

Lyophilized from a 0.2 μm filtered solution of 10 mM NaAC, 40 mM Arg, 0.12mg/ml Met, 146mg/ml Sucrose, 0.1% PF-68, pH 4.5 or PBS, pH 7.4, 8% trehalose.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O.

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.