NMI — N-myc and STAT interactor
NMI belongs to a gene co-expression module in 4 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
NMI's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD4⁺ T cells | Th17 lineage Th17 fate | ADA, ARHGEF3, CD226, CD52, DENND3, EVL, IDH2, IL17RE +13 more | View in SCUBA |
| CD8⁺ T cells | Type I Interferon Inflammation | BST2, CHMP5, EIF2AK2, LAP3, NAPA, OASL, PLSCR1, SPATS2L +1 more | View in SCUBA |
| Macrophages | Immunoproteasome Induction Inflammatory | CBR1, DAPP1, DYNLT1, EPSTI1, IFI35, LAP3, LGALS9, LYSMD2 +12 more | View in SCUBA |
| Mucosal-associated invariant T cell | Type I Interferon Inflammation | APOL2, CHMP5, COMMD8, FBXO6, GBP1, PARP9, RBCK1, RIGI +9 more |
About the gene
| Chromosome | 2: 151270470-151289894 |
|---|---|
| Predicted location | Intracellular, Secreted |
| Essential gene | No |
| Protein class | Plasma proteins, Predicted intracellular proteins, Predicted secreted proteins |
| Biological process | Host-virus interaction, Immunity, Innate immunity |
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 (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. 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.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.