Anti-Recombinant-NMI antibody [RM1B09] (STJA0026779)

SPECIFICATIONS
ClonalityMonoclonal
HostRabbit
ConjugationUnconjugated
IsotypeIgG
STJA0026779
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General Information

Short DescriptionRabbit monoclonal anti-Recombinant-N-Myc-Interactor for use in IF, IHC, IP and WB in Human samples. Datasheet included with dilution recommendations, and related reagents.
ApplicationsIF/IHC/IP/WB
HostRabbit
ReactivityHuman
NoteSTRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.

Product Properties

ClonalityMonoclonal
Clone IDRM1B09
IsotypeIgG
ConjugationUnconjugated
PurificationProtein A/G purified from cell culture supernatant
Dilution RangeIF: 1:50-1:200, IHC: 1:100-1:200, IP: 1:20-1:50, WB: 1:1000-1:2000
Formulation0.01M PBS, pH 7.4, 0.05% BSA, 50% Glycerol, 0.05% Sodium Azide
Storage InstructionSuitable for storage at +4°C between 1-2 weeks. For longer term store at-20°C for up to 12 months.

Target Information

Gene SymbolNMI
Gene ID9111
Uniprot IDNMI_HUMAN

Additional Info

Post Translational Modifications Ubiquitinated. 'Lys-63'-linked ubiquitination by TRIM21 promotes interaction with IFI35 and inhibits virus-triggered type I IFN-beta production.
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 pro-inflammatory cytokines.
Protein Name N-Myc-Interactor
Nmi
N-Myc And Stat Interactor
Database Links Reactome: R-HSA-9692916
Cellular Localisation Cytoplasm
Nucleus
Secreted
Cytoplasmic Nmi Localizes In Punctate Granular Structures
Nuclear Localization Increased Following Ifn-Alpha Treatment
Extracelullar Following Secretion By Macrophage
Alternative Antibody Names Anti-N-Myc-Interactor antibody
Anti-Nmi antibody
Anti-N-Myc And Stat Interactor antibody
Anti-NMI antibody

Information sourced from Uniprot.org

Citations

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