I9032
Interferon β from mouse
≥95%, recombinant, expressed in E. coli, buffered aqueous solution, suitable for cell culture
Synonym(s):
IFN β
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About This Item
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biological source
mouse
Quality Level
recombinant
expressed in E. coli
Assay
≥95%
form
buffered aqueous solution
mol wt
~20 kDa
packaging
pkg of 1 vial
concentration
2560000 units/mL
technique(s)
cell culture | mammalian: suitable
UniProt accession no.
shipped in
dry ice
storage temp.
−70°C
Gene Information
mouse ... Ifnb1(15977)
Related Categories
General description
IFN β (interferon β) is from the type 1 interferon family of cytokines.
Interferon β (IFN-β) possesses a signal peptide region. It has comparatively more hydrophobic residues and displays 30% homology with IFN-α.
The gene encoding interferon β (Infb1) is localized on mouse chromosome 4.
Application
Interferon β from mouse has been used:
- in the stimulation of bone marrow-derived dendritic cells (BMDCs)
- as a cytokine to stimulate differentiation of podocytes
- to stimulate splenocytes
Interferon ß from mouse has been used:
- to induce the activation of cholesterol 25-hydroxylase, by in vitro stimulation of bone marrow-derived macrophages, dendritic cells and CD11c+ lung macrophages
- to stimulate splenocytes, in order to study the secretion and regulation of IFN-γ
- to intranasally pre-treat neonatal mice, to study its effects on the protective actions of Lactobacillus rhamnosus GG (LGG)
- as a standard to treat MEF-Mx2-luc-BKO reporter cell line for IFN-β measurement, in response to human adenovirus-5 (HAdV-C5)
Biochem/physiol Actions
In presence of virus infection, IFN β (interferon β) is upregulated and plays a crucial role in innate antiviral response. It is also important for anti-inflammatory effects.
Interferon β (IFN-β) suppresses a variety of proinflammatory cytokines in lymphocytes including the interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α). It also favors the synthesis of antagonists associated with interleukin IL-10 and IL-1 receptor. IFN-β downregulates interferon γ production but enhances transforming growth factor β1 expression. It has therapeutic potential in treating rheumatoid arthritis and relapsing-remitting multiple sclerosis (MS).
Interferon β has a role in the activation of human leukocyte antigen (HLA) gene expression. It acts as a messenger during bacterial infections.
Cytokine with anti-viral, anti-proliferative, immunoregulatory, and proinflammatory activities.
Physical form
Solution in 20 mM HEPES, pH 6.0, 0.5 M NaCl, 6% glycerol, and 0.1% bovine serum albumin.
Analysis Note
The biological activity is determined in the cytopathic effect inhibition assay using mouse L929 cells with encephalomyocarditis virus. The cytopathic effect of 50% is produced with approximately 1 unit/ml interferon. The units are determined with respect to NIH international standard reference for mouse interferon β.
Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Patrick Ejlerskov et al.
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Neurodegenerative diseases have been linked to inflammation, but whether altered immunomodulation plays a causative role in neurodegeneration is not clear. We show that lack of cytokine interferon-β (IFN-β) signaling causes spontaneous neurodegeneration in the absence of neurodegenerative disease-causing mutant proteins.
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P Keskinen et al.
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HLA class I and II molecules play a central role in regulating host immune responses against microbial infections because they present foreign antigens to CD8+ and CD4+ T lymphocytes, respectively. Many cytokines, especially interferons (IFN), are known to upregulate human
Nanthapon Ruangkiattikul et al.
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Type I interferons (IFN-I), such as IFN-α and IFN-β are important messengers in the host response against bacterial infections. Knowledge about the role of IFN-I in infections by nontuberculous mycobacteria (NTM) is limited. Here we show that macrophages infected with
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Podocytes are terminally differentiated renal cells, lacking the ability to regenerate by proliferation. However, during renal injury, podocytes re-enter into the cell cycle but fail to divide. Earlier studies suggested that re-entry into cell cycle results in loss of podocytes
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