Leukocyte IFN, B cell IFN, Type I IFN, IFNB1, IFB, IFF, IFNB, IFN-b 1b, MGC96956.
IFN beta Mouse Recombinant produced in E.Coli is a single, non-glycosylated polypeptide chain containing 182 amino acids (22-182 a.a.) and having a molecular mass of 22 kDa. Mouse IFN beta is fused to 21 amino acid at N-terminus and purified by proprietary chromatographic techniques.
Leukocyte IFN, B cell IFN, Type I IFN, IFNB1, IFB, IFF, IFNB, IFN-b 1b, MGC96956.
MGSSHHHHHH SSGLVPRGSH MINYKQLQLQ ERTNIRKCQE LLEQLNGKIN LTYRADFKIP MEMTEKMQKS YTAFAIQEML QNVFLVFRNN FSSTGWNETI VVRLLDELHQ QTVFLKTVLE EKQEERLTWE MSSTALHLKS YYWRVQRYLK LMKYNSYAWM VVRAEIFRNF LIIRRLTRNF QN.
Recombinant Mouse IFN-β (His Tag) is a mouse full-length protein expressed in HEK 293 cells . The recombinant protein is typically produced in a non-glycosylated form and contains a His tag at the C-terminus, which facilitates its purification and detection . The molecular mass of the recombinant protein is approximately 22 kDa .
IFN-β is part of the type I IFN multigene family, which includes several subtypes such as IFN-α, IFN-ε, IFN-κ, IFN-ω, IFN-τ, IFN-δ, and IFN-ζ . Type I interferons are expressed as a first line of defense against viruses and play a critical role in the antiviral response. They exert their antiviral activity through various mechanisms, including blocking viral entry into cells, controlling viral transcription, cleaving RNA, and preventing translation .
In addition to its antiviral properties, IFN-β modulates both innate and adaptive immune responses. It induces natural killer cell cytotoxicity, enhances the expression of major histocompatibility complex class I molecules on most cells, and upregulates costimulatory molecules on antigen-presenting cells . IFN-β also acts directly on CD8 T cells to promote clonal expansion and memory formation in response to viral infections .
Recombinant Mouse IFN-β (His Tag) is widely used in various research applications, including:
IFN-β has been used in the treatment of multiple sclerosis (MS) in humans. It has been suggested that IFN-β inhibits the differentiation of human Th17 cells, which play a central role in the immunopathogenesis of MS . Animal studies have shown that mice deficient in the type I IFN receptor (IFNAR) have increased susceptibility to experimental autoimmune encephalomyelitis (EAE), a model for MS .