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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. De plus, nous expédions NMI Anticorps (50) et NMI Protéines (9) et beaucoup plus de produits pour cette protéine.
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results provide new insights into understanding the regulatory mechanism of cancer stem cells and suggest that the NMI-YY1 (Montrer YY1 Kits ELISA)-hTERT signaling axis may be a potential therapeutic target for breast cancers.
Damage-associated molecular patterns (DAMP (Montrer AMPH Kits ELISA)) are important mediators of innate immunity. Here the authors show that N-myc and STAT interactor (NMI) and interferon-induced protein 35 (IFP35 (Montrer IFI35 Kits ELISA)) act as DAMPs to promote inflammation by activating macrophages via the Toll-like receptor 4 (Montrer TLR4 Kits ELISA) and NF-kappaB (Montrer NFKB1 Kits ELISA) pathways.
These investigations demonstrated etoposide-induced NMI can suppress tumor proliferation and promote cell apoptosis by activating the ARF-p53 (Montrer TP53 Kits ELISA) 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 (Montrer MAPK3 Kits ELISA)/2 activation, and thereby further evoke malignant progression of hepatocellular carcinoma (HCC).
N-Myc (Montrer MYCN Kits ELISA)-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-kappaB (Montrer NFKB1 Kits ELISA)/p65 in histone deacetylase (Montrer HDAC1 Kits ELISA)-dependent manner.
N-myc and STAT interactor sensitizes breast cancer cells to cisplatin treatment through DRAM1 (Montrer DRAM1 Kits ELISA) dependent autophagy.
Results show that aberrant miR (Montrer MLXIP Kits ELISA)-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.
overexpression or depletion of NMI revealed its regulation on G1/S progression and cell proliferation (both in vitro and in vivo), and this effect was partially dependent on STAT1 (Montrer STAT1 Kits ELISA), which interacted with and was regulated by NMI.
Trim21 (Montrer TRIM21 Kits ELISA) regulates Nmi-IFI35 (Montrer IFI35 Kits ELISA) complex-mediated inhibition of innate antiviral response
These findings suggest that Nmi is a negative regulator of the virus-triggered induction of type I IFNs that targets IRF7 (Montrer IRF7 Kits ELISA)
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