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IFN-beta Antibody

     
  • 1 - IFN-beta Antibody ASC10546
    Western blot analysis of IFN-b in A-20 cell lysate with IFN-b antibody at 5 µg/mL.
  • 2 - IFN-beta Antibody ASC10546
    Immunohistochemistry of IFN-b in human liver tissue with IFN-b antibody at 5 µg/mL.
  • 3 - IFN-beta Antibody ASC10546
    Immunofluorescence of IFN-beta in Human Liver cells with IFN-beta antibody at 20 µg/mL.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, IF, E, IHC-P
Primary Accession P01574
Other Accession AAC41702, 184623
Reactivity Human, Mouse
Host Rabbit
Clonality Polyclonal
Isotype IgG
Calculated MW 22294 Da
Concentration (mg/ml) 1 mg/mL
Conjugate Unconjugated
Application Notes IFN-b antibody can be used for detection of IFN-b by Western blot at 5 µg/mL. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL.
Additional Information
Gene ID 3456
Other Names Interferon beta, IFN-beta, Fibroblast interferon, IFNB1, IFB, IFNB
Target/Specificity IFNB1;
Reconstitution & Storage IFN-beta antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
PrecautionsIFN-beta Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name IFNB1 (HGNC:5434)
Synonyms IFB, IFNB
Function Type I interferon cytokine that plays a key role in the innate immune response to infection, developing tumors and other inflammatory stimuli (PubMed:10049744, PubMed:10556041, PubMed:6157094, PubMed:6171735, PubMed:7665574, PubMed:8027027, PubMed:8969169). Signals via binding to high-affinity (IFNAR2) and low-affinity (IFNAR1) heterodimeric receptor, activating the canonical Jak-STAT signaling pathway resulting in transcriptional activation or repression of interferon-regulated genes that encode the effectors of the interferon response, such as antiviral proteins, regulators of cell proliferation and differentiation, and immunoregulatory proteins (PubMed:10049744, PubMed:10556041, PubMed:7665574, PubMed:8027027, PubMed:8969169). Signals mostly via binding to a IFNAR1-IFNAR2 heterodimeric receptor, but can also function with IFNAR1 alone and independently of Jak-STAT pathways (By similarity). Elicits a wide variety of responses, including antiviral and antibacterial activities, and can regulate the development of B-cells, myelopoiesis and lipopolysaccharide (LPS)- inducible production of tumor necrosis factor (By similarity). Plays a role in neuronal homeostasis by regulating dopamine turnover and protecting dopaminergic neurons: acts by promoting neuronal autophagy and alpha-synuclein clearance, thereby preventing dopaminergic neuron loss (By similarity). IFNB1 is more potent than interferon-alpha (IFN- alpha) in inducing the apoptotic and antiproliferative pathways required for control of tumor cell growth (By similarity).
Cellular Location Secreted.
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

IFN-beta Antibody: Type I Interferons (IFN-alpha/beta) are produced primarily in response to viral infection by "Natural IFN-producing cells" (IPCs) as part of the host immune response and can also inhibit the development of tumors. IFN-beta binding by its receptor results in the activation of the tyrosine kinases Jak1 and Tyk2 and phosphorylation of members of the STAT family of transcription factors, leading to the transcription and expression of the immune response genes. More recently, several members of the toll-like receptor (TLR) family were found to stimulate the production IFN-beta. IFN-beta is currently used clinically for treatment of tumors, infections and multiple sclerosis.

REFERENCES

Gresser I. Wherefore interferon? J. Leuk. Biol.1997; 61:567-74.
Colonna M. TLR pathways and IFN-regulatory factors: to each its own. Eur. J. Immunol.2007; 37:306-9.
Kock M, Mostert J, De Keyser J, et al. Interferon-beta treatment and the natural history of relapsing-remitting multiple sclerosis. Ann. Neurol.2007; epub.

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