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Human N-myc-interactor(NMI) ELISA kit

  • 中文名称:
    人N-Myc互作蛋白(NMI)酶联免疫试剂盒
  • 货号:
    CSB-EL015893HU
  • 规格:
    96T/48T
  • 价格:
    ¥3600/¥2500
  • 其他:

产品详情

  • 产品描述:

    This Human NMI ELISA Kit was designed for the quantitative measurement of Human NMI protein in serum, plasma, tissue homogenates, cell lysates. It is a Sandwich ELISA kit, its detection range is 23.5 pg/mL-1500 pg/mL and the sensitivity is 5.8 pg/mL.

  • 别名:
    NMI ELISA Kit; N-myc-interactor ELISA Kit; Nmi ELISA Kit; N-myc and STAT interactor ELISA Kit
  • 缩写:
    NMI
  • Uniprot No.:
  • 种属:
    Homo sapiens (Human)
  • 样本类型:
    serum, plasma, tissue homogenates, cell lysates
  • 检测范围:
    23.5 pg/mL-1500 pg/mL
  • 灵敏度:
    5.8 pg/mL
  • 反应时间:
    1-5h
  • 样本体积:
    50-100ul
  • 检测波长:
    450 nm
  • 研究领域:
    Epigenetics and Nuclear Signaling
  • 测定原理:
    quantitative
  • 测定方法:
    Sandwich
  • 精密度:
    Intra-assay Precision (Precision within an assay): CV%<8%
    Three samples of known concentration were tested twenty times on one plate to assess.
    Inter-assay Precision (Precision between assays): CV%<10%
    Three samples of known concentration were tested in twenty assays to assess.
  • 线性度:
    To assess the linearity of the assay, samples were spiked with high concentrations of human NM in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
      Sample Serum(n=4)
    1:1 Average % 104
    Range % 100-108
    1:2 Average % 89
    Range % 86-92
    1:4 Average % 106
    Range % 103-109
    1:8 Average % 98
    Range % 94-102
  • 回收率:
    The recovery of human NM spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
    Sample Type Average % Recovery Range
    Serum (n=5) 85 81-89
    EDTA plasma (n=4) 93 90-96
  • 标准曲线:
    These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
    pg/ml OD1 OD2 Average Corrected
    1500 2.660 2.701 2.681 2.587
    750 2.318 2.203 2.261 2.167
    375 1.676 1.698 1.687 1.593
    187.5 1.065 1.104 1.085 0.991
    94 0.643 0.675 0.659 0.565
    47 0.431 0.442 0.437 0.343
    23.5 0.271 0.281 0.276 0.182
    0 0.093 0.095 0.094  
  • 数据处理:
  • 货期:
    3-5 working days

产品评价

靶点详情

  • 功能:
    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.
  • 基因功能参考文献:
    1. These results revealed that IRF-1 is involved in the IFN-inducible expression of Nmi. PMID: 28913576
    2. Our study showed that NMI suppressed tumor growth by inhibiting PI3K/AKT, MMP2/MMP9, COX-2/PGE2 signaling pathways and p300-mediated NF-kappaB acetylation, and predicted a favorable prognosis in human lung adenocarcinomas, suggesting that NMI was a potential tumor suppressor in lung cancer. PMID: 29025423
    3. results provide new insights into understanding the regulatory mechanism of cancer stem cells and suggest that the NMI-YY1-hTERT signaling axis may be a potential therapeutic target for breast cancers. PMID: 28492540
    4. Damage-associated molecular patterns (DAMP) are important mediators of innate immunity. Here the s show that N-myc and STAT interactor (NMI) and interferon-induced protein 35 (IFP35) act as DAMPs to promote inflammation by activating macrophages via the Toll-like receptor 4 and NF-kappaB pathways. PMID: 29038465
    5. These investigations demonstrated etoposide-induced NMI can suppress tumor proliferation and promote cell apoptosis by activating the ARF-p53 signaling pathway in lung carcinoma. Our results provide an alternative mechanism for etoposide in lung carcinoma and suggest NMI has a critical role in suppressing lung carcinoma progression. PMID: 29030066
    6. Data suggest that N-myc (and STAT) interactor (NMI) could improve its downstream target bradykinin B2 receptor (BDKRB2) expression to induce extracellular signal-regulated kinases (ERK) 1/2 activation, and thereby further evoke malignant progression of hepatocellular carcinoma (HCC). PMID: 28077802
    7. N-Myc-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-kappaB/p65 in histone deacetylase-dependent manner. PMID: 27012186
    8. N-myc and STAT interactor sensitizes breast cancer cells to cisplatin treatment through DRAM1 dependent autophagy. PMID: 26146406
    9. Results show that aberrant miR-29 expression may account for reduced NMI expression in breast tumors and mesenchymal phenotype of cancer cells that promotes invasive growth. PMID: 25174825
    10. The results showed that SARS coronavirus protein 6 can promote the ubiquitin-dependent proteosomal degradation of Nmi. PMID: 25907116
    11. overexpression or depletion of NMI revealed its regulation on G1/S progression and cell proliferation (both in vitro and in vivo), and this effect was partially dependent on STAT1, which interacted with and was regulated by NMI. PMID: 25669971
    12. Trim21 regulates Nmi-IFI35 complex-mediated inhibition of innate antiviral response PMID: 26342464
    13. Its potential function in transcriptional activation of NMI. PMID: 25387807
    14. identified NMI induction as a novel negative feedback mechanism that decreases IRE1alpha-dependent activation of JNK and apoptosis in cytokine-exposed beta cells PMID: 24936061
    15. Thus our work reveals a novel NMI-mediated, transcription-independent ARF induction pathway in response to cellular stresses. PMID: 23034180
    16. Dissociation of the IFN-induced protein NMI from IFP35 is a newly defined specific cytoplasmic event occurring during apoptosis. PMID: 11911807
    17. complex with BRCA1 and c-Myc inhibits c-Myc-induced human telomerase reverse transcriptase gene promoter activity in breast cancer PMID: 11916966
    18. Apoptin mutant T1 still interacted with Nmi, suggesting that its C-terminal 11 AA was not essential for the interaction. PMID: 12019454
    19. STAT1 and Nmi are downstream targets of Ets-1 in MCF-7 human breast cancer cells PMID: 15996661
    20. identified an association of Sox10 with the N-myc interactor Nmi, which was mediated by the high-mobility group of Sox10 and the central region of Nmi; Nmi modulated the transcriptional activity of Sox10 PMID: 16214168
    21. The results provide a novel role of CKIP-1 in cytokine signaling response and the biochemical mechanism, by which two previously identified modulators IFP35 and Nmi are involved via interactions. PMID: 17197158
    22. Activation of PKCdelta in response to Camptothecin treatment requires Myc and is important in CPT-mediated apoptosis signaling. PMID: 17565738
    23. Data suggest that overexpression of Nmi inhibits the Wnt/beta-catenin signaling via up-regulation of Dkk1 and retards tumor growth. PMID: 19358268

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  • 亚细胞定位:
    Cytoplasm. Nucleus. Secreted.
  • 蛋白家族:
    NMI family
  • 组织特异性:
    Expressed in adult spleen, liver, and kidney. Expressed in fetal thymus, liver, placenta, spleen, lung, and kidney but not brain. Expressed in macrophages.
  • 数据库链接:

    HGNC: 7854

    OMIM: 603525

    KEGG: hsa:9111

    STRING: 9606.ENSP00000243346

    UniGene: Hs.54483