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

IFNA1 (Interferon Alpha 1, also known as IFL; IFN; IFNA@; IFNA13; Leif D; IFN-ALPHA; IFN-alphaD), located on 9p21.3, is a Protein Coding gene. The gene produces a 21725 Da protein composed of 189 amino acids. IFNA1 is produced by macrophages and has antiviral activities. It belongs to the alpha/beta interferon family. Diseases such as Hepatitis and Viral Infectious Disease are associated with IFNA1. The related pathways of IFNA1 include all-trans-retinoic Acid Mediated Apoptosis and Tuberculosis.

Interferon alpha 1/IFNA1 Protein (4)

    Interferon alpha 1/IFNA1 Antibody (2)

      Interferon alpha 1/IFNA1 cDNA Clone (26)


      Interferon alpha 1/IFNA1 Lysate (2)

        Interferon alpha 1/IFNA1 Background

        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 the 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 References

        • 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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