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Recombinant Human N-myc-interactor (NMI)

ACP18176

Number
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High Purity LevelsPrecision and ReliabilityCustomization Options

Specifications


Cat.No ACP18176 Target NameNMI
Target SynonymsNMI; N-myc-interactor; Nmi; N-myc and STAT interactorFormLyophilized powder
Expression SystemCustom Production. Please inquire and provide the desire expression system.Expression Range1-307
Protein LengthFull length proteinPurity>85% (SDS-PAGE)
Storage Buffer5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0.

Immunogen Information


Target SpeciesHumanUniprot IDQ13287
Background Information
  • Uniprot Id

    Q13287

  • Target Species

    Human

  • Target Name

    NMI

  • Target Full Name

    N-myc-interactor

  • Target Function

    Acts as a signaling pathway regulator involved in innate immune system response. In response to interleukin 2/IL2 and interferon IFN-gamma/IFNG, interacts with signal transducer and activator of transcription/STAT which activate the transcription of downstream genes involved in a multitude of signals for development and homeostasis. Enhances the recruitment of CBP/p300 coactivators to STAT1 and STAT5, resulting in increased STAT1- and STAT5-dependent transcription. In response to interferon IFN-alpha, associates in a complex with signaling pathway regulator IFI35 to regulate immune response; the complex formation prevents proteasome-mediated degradation of IFI35. In complex with IFI35, inhibits virus-triggered type I IFN-beta production when ubiquitinated by ubiquitin-protein ligase TRIM21. In complex with IFI35, negatively regulates nuclear factor NF-kappa-B signaling by inhibiting the nuclear translocation, activation and transcription of NF-kappa-B subunit p65/RELA, resulting in the inhibition of endothelial cell proliferation, migration and re-endothelialization of injured arteries. Negatively regulates virus-triggered type I interferon/IFN production by inducing proteosome-dependent degradation of IRF7, a transcriptional regulator of type I IFN, thereby interfering with cellular antiviral responses. Beside its role as an intracellular signaling pathway regulator, also functions extracellularly as damage-associated molecular patterns (DAMPs) to promote inflammation, when actively released by macrophage to the extracellular space during cell injury or pathogen invasion. Macrophage-secreted NMI activates NF-kappa-B signaling in adjacent macrophages through Toll-like receptor 4/TLR4 binding and activation, thereby inducing NF-kappa-B translocation from the cytoplasm into the nucleus which promotes the release of proinflammatory cytokines.

  • Target Subcellular Location

    Cytoplasm. Nucleus. Secreted.

  • Target Protein Families

    NMI family

  • Target Tissue Specificity

    Expressed in adult spleen, liver, and kidney. Expressed in fetal thymus, liver, placenta, spleen, lung, and kidney but not brain. Expressed in macrophages.

  • Target Research Area

    Epigenetics and Nuclear Signaling

  • Target Synonyms

    NMI; N-myc-interactor; Nmi; N-myc and STAT interactor

  • Target Background

    NMYC interactor (NMI) encodes a protein that interacts with NMYC and CMYC (two members of the oncogene Myc family), and other transcription factors containing a Zip, HLH, or HLH-Zip motif. The NMI protein also interacts with all STATs except STAT2 and augments STAT-mediated transcription in response to cytokines IL2 and IFN-gamma. The NMI mRNA has low expression levels in all human fetal and adult tissues tested except brain and has high expression in cancer cell line-myeloid leukemias.

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