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NMI Antibody (clone 9D8)
Mouse Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | Q13287 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Clone Names | 9D8 |
| Calculated MW | 35kDa |
| Dilution | IHC-P (5 µg/ml) |
| Gene ID | 9111 |
|---|---|
| Other Names | N-myc-interactor, Nmi, N-myc and STAT interactor, NMI |
| Reconstitution & Storage | Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. |
| Precautions | NMI Antibody (clone 9D8) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | NMI (HGNC:7854) |
|---|---|
| Function | Acts as a signaling pathway regulator involved in innate immune system response (PubMed:9989503, PubMed:26342464, PubMed:29038465, PubMed:29350881). 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 (PubMed:9989503, PubMed:29377960). Enhances the recruitment of CBP/p300 coactivators to STAT1 and STAT5, resulting in increased STAT1- and STAT5-dependent transcription (PubMed:9989503). 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 (PubMed:10779520, PubMed:10950963). In complex with IFI35, inhibits virus-triggered type I IFN-beta production when ubiquitinated by ubiquitin-protein ligase TRIM21 (PubMed:26342464). 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 (PubMed:29350881). 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 (By similarity). 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 (PubMed:29038465). 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 pro- inflammatory cytokines (PubMed:29038465). |
| Cellular Location | Cytoplasm. Nucleus. Secreted Note=Cytoplasmic NMI localizes in punctate granular structures (PubMed:9781816, PubMed:10950963). Nuclear localization increased following IFN-alpha treatment (PubMed:9781816, PubMed:10950963) Extracelullar following secretion by macrophage (PubMed:29038465) |
| Tissue Location | Expressed in adult spleen, liver, and kidney (PubMed:9781816). Expressed in fetal thymus, liver, placenta, spleen, lung, and kidney but not brain (PubMed:9781816). Expressed in macrophages (PubMed:29038465). |
Citations (0)
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info@abcepta.com, and receive a free "I Love Antibodies" mug.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
Background
May be involved in augmenting coactivator protein recruitment to a group of sequence-specific transcription factors. Augments cytokine-mediated STAT transcription. Enhances CBP/p300 coactivator protein recruitment to STAT1 and STAT5.
References
Bao J.,et al.Oncogene 12:2171-2176(1996).
Goshima N.,et al.Nat. Methods 5:1011-1017(2008).
Hillier L.W.,et al.Nature 434:724-731(2005).
Mural R.J.,et al.Submitted (SEP-2005) to the EMBL/GenBank/DDBJ databases.
Zhu M.-H.,et al.Cell 96:121-130(1999).
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