IL3 Mouse, sf9 binds to high-affinity receptors composed of α and β subunits (AIC2A/AIC2B in mice), triggering signaling pathways that regulate:
Hematopoiesis: Supports growth of myeloid precursors, mast cells, eosinophils, and basophils .
Neurotrophic Activity: Modulates microglial function in neurodegenerative diseases like Alzheimer’s .
Immune Regulation: Amplifies inflammatory responses in autoimmune diseases (e.g., lupus, multiple sclerosis) .
Studies in A/J mice revealed that defects in IL-3 receptor α-subunit splicing impair hematopoietic colony formation, underscoring IL-3’s non-redundant role in hematopoiesis .
Cell Proliferation Assays: ED50 < 0.1 ng/mL in TF-1 cell lines, indicating high specific activity (10,000,000 IU/mg) .
Receptor Binding Studies: Structural analyses of IL-3Rα/β complexes reveal two distinct binding modes critical for signaling .
Neurodegeneration: IL-3 reprograms microglia to clear amyloid-β aggregates in Alzheimer’s models but exacerbates neuroinflammation in multiple sclerosis .
Autoimmunity: Elevated IL-3 correlates with lupus nephritis severity and IFNα production in SLE patients .
Structural Biology: The IL-3Rα N-terminal domain (NTD) dynamically regulates cytokine binding and protects against aberrant signaling .
Dual Receptor System: Mice employ two β-subunits (AIC2A/AIC2B) to form high-affinity IL-3 receptors, unlike humans .
Therapeutic Implications: Targeting IL-3/CD123 axis shows potential in autoimmune diseases but risks hematologic toxicity .
Interleukin-3 (Mouse Recombinant, sf9) is produced in Sf9 Baculovirus cells. The recombinant IL-3 is a single, glycosylated polypeptide chain containing 148 amino acids (27-166 a.a.) and has a molecular mass of 16.7 kDa. Under reducing conditions, it migrates at 18-28 kDa on SDS-PAGE . The protein is expressed with a 6 amino acid His tag at the C-terminus and is purified using proprietary chromatographic techniques .
The amino acid sequence of Interleukin-3 (Mouse Recombinant, sf9) is as follows:
ASISGRDTHR LTRTLNCSSI VKEIIGKLPE PELKTDDEGP SLRNKSFRRV NLSKFVESQG
EVDPEDRYVI KSNLQKLNCC LPTSANDSAL PGVFIRDLDD FRKKLRFYMV HLNDLETVLT
SRPPQPASGS VSPNRGTVEC LEHHHHHH