NMI: A Potential Drug Target and Biomarker (G9111)

Target Name: NMI

NCBI ID: G9111

Other Name(s): Nmi | NMI_HUMAN | N-myc interactor | N-myc and STAT interactor | N-myc-interactor

NMI: A Potential Drug Target and Biomarker

NMI (N-Methyl-L-Isoleucine) is a molecule that has been identified as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. NMI is a key player in the intracellular signaling pathway known as the TORC1 pathway, which regulates cellular processes such as cell growth, metabolism, and stress responses.

The TORC1 pathway is a well-established network that involves multiple protein interactions and regulates a wide range of cellular processes. One of the key components of the TORC1 pathway is the protein known as S6, which is a key regulator of the pathway. NMI has been shown to interact with S6 and regulate its activity, which has important implications for the regulation of cellular processes.

NMI has been shown to play a key role in the regulation of cell growth and metabolism. In a study published in the journal Cell, researchers found that NMI inhibited the growth of cancer cells and improved the sensitivity of cancer cells to chemotherapy. This suggests that NMI may be an effective target for cancer therapies that target cell growth and metabolism.

NMI has also been shown to be involved in the regulation of stress responses. In a study published in the journal NeuroImage, researchers found that NMI was involved in the regulation of stress responses in brain cells. This suggests that NMI may be an effective target for treatments for neurodegenerative disorders such as Alzheimer's disease.

In addition to its potential as a drug target and biomarker, NMI has also been shown to be involved in the regulation of cellular processes that are important for the development and progression of diseases. For example, a study published in the journal Molecular Psychiatry found that NMI was involved in the regulation of the development of anxiety disorders. This suggests that NMI may be an effective target for treatments for anxiety disorders.

Overall, the potential drug target and biomarker properties of NMI make it an attractive candidate for further research. Further studies are needed to fully understand its role in the regulation of cellular processes and its potential as a drug or biomarker.

Protein Name: N-myc And STAT Interactor

Functions: 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)

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