Interferon alpha 1/IFNA1 Proteins, Antibodies, cDNA Clones Research Reagents

All Interferon alpha 1/IFNA1 reagents are produced in house and quality controlled, including 2 Interferon alpha 1/IFNA1 Antibody, 26 Interferon alpha 1/IFNA1 Gene, 2 Interferon alpha 1/IFNA1 Lysate, 4 Interferon alpha 1/IFNA1 Protein, 3 Interferon alpha 1/IFNA1 qPCR. All Interferon alpha 1/IFNA1 reagents are ready to use.

Interferon alpha 1/IFNA1 Protein (4)

    Interferon alpha 1/IFNA1 Antibody (2)

      Interferon alpha 1/IFNA1 cDNA Clone (26)


      クローニングベクター cDNA 製品

      In lentiviral vector


      クローニングベクター cDNA 製品

      In lentiviral vector

      Interferon alpha 1/IFNA1 Lysate (2)

        Interferon alpha 1/IFNA1 の背景知識

        IFNA1, also known as IFN-alpha and IFNA, belongs to the alpha/beta interferon family. Interferons(IFNs) are proteins made and released by host cells in response to the presence of pathogens such as viruses, bacteria, parasites or tumor cells. They belong to the large class of glycoproteins known as cytokines. IFNs stimulate the production of two enzymes: a protein kinase and an oligoadenylate synthetase. They allow for communication between cells to trigger the protective defenses of the immune system that eradicate pathogens or tumors. IFNs can activate immune cells, such as natural killer cells and macrophages; they increase recognition of infection or tumor cells by up-regulating antigen presentation to T lymphocytes; and they also increase the ability of uninfected host cells to resist new infection by virus.Leukocyte interferon is produced predominantly by B lymphocytes. Immune interferon is produced by mitogen- or antigen-stimulated T lymphocytes. IFNA1 is produced by macrophages and has antiviral activities.

        Interferon alpha 1/IFNA1 の参考文献

        • Takayama I, et al. (2012) The nucleocapsid protein of measles virus blocks host interferon response. Virology. 424(1):45-55.
        • Vairo D, et al. (2011) Severe impairment of IFN-? and IFN-? responses in cells of a patient with a novel STAT1 splicing mutation. Blood. 118(7):1806-17.
        • Bhattacharya S, et al. (2011) Bcr-abl signals to desensitize chronic myeloid leukemia cells to IFN? via accelerating the degradation of its receptor. Blood. 118(15):4179-87.

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