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NMYC interactor (NMI) encodes a protein that interacts with NMYC and CMYC (two members of the oncogene Myc family), and other transcription factors containing a Zip, HLH, or HLH-Zip motif. Additionally we are shipping NMI Antibodies (58) and NMI Proteins (9) and many more products for this protein.
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These results revealed that IRF-1 (show IRF1 ELISA Kits) is involved in the IFN-inducible expression of Nmi.
Our study showed that NMI suppressed tumor growth by inhibiting PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits), MMP2 (show MMP2 ELISA Kits)/MMP9 (show MMP9 ELISA Kits), COX-2 (show COX2 ELISA Kits)/PGE2 signaling pathways and p300 (show EP300 ELISA Kits)-mediated NF-kappaB (show NFKB1 ELISA Kits) acetylation, and predicted a favorable prognosis in human lung adenocarcinomas, suggesting that NMI was a potential tumor suppressor in lung cancer.
results provide new insights into understanding the regulatory mechanism of cancer stem cells and suggest that the NMI-YY1 (show YY1 ELISA Kits)-hTERT signaling axis may be a potential therapeutic target for breast cancers.
Damage-associated molecular patterns (DAMP (show AMPH ELISA Kits)) are important mediators of innate immunity. Here the authors show that N-myc and STAT interactor (NMI) and interferon-induced protein 35 (IFP35 (show IFI35 ELISA Kits)) act as DAMPs to promote inflammation by activating macrophages via the Toll-like receptor 4 (show TLR4 ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits) pathways.
These investigations demonstrated etoposide-induced NMI can suppress tumor proliferation and promote cell apoptosis by activating the ARF-p53 (show TP53 ELISA Kits) 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.
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 (show MAPK3 ELISA Kits)/2 activation, and thereby further evoke malignant progression of hepatocellular carcinoma (HCC).
N-Myc (show MYCN ELISA Kits)-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-kappaB (show NFKB1 ELISA Kits)/p65 in histone deacetylase (show HDAC1 ELISA Kits)-dependent manner.
N-myc and STAT interactor sensitizes breast cancer cells to cisplatin treatment through DRAM1 (show DRAM1 ELISA Kits) dependent autophagy.
Results show that aberrant miR (show MLXIP ELISA Kits)-29 expression may account for reduced NMI expression in breast tumors and mesenchymal phenotype of cancer cells that promotes invasive growth.
The results showed that SARS coronavirus protein 6 can promote the ubiquitin-dependent proteosomal degradation of Nmi.
These findings suggest that Nmi is a negative regulator of the virus-triggered induction of type I IFNs that targets IRF7 (show IRF7 ELISA Kits)
NMYC interactor (NMI) encodes a protein that interacts with NMYC and CMYC (two members of the oncogene Myc family), and other transcription factors containing a Zip, HLH, or HLH-Zip motif. The NMI protein also interacts with all STATs except STAT2 and augments STAT-mediated transcription in response to cytokines IL2 and IFN-gamma. The NMI mRNA has low expression levels in all human fetal and adult tissues tested except brain and has high expression in cancer cell line-myeloid leukemias.
, N-mcy (and STAT) interactor
, N-myc (and STAT) interactor
, N-myc and STAT interactor
, N-myc/STAT interactor