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NDRG1 is a member of the N-myc downregulated gene family which belongs to the alpha/beta hydrolase superfamily. De plus, nous expédions N-Myc Downstream Regulated 1 Anticorps (165) et N-Myc Downstream Regulated 1 Protéines (16) et beaucoup plus de produits pour cette protéine.
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NDRG1 over-expression promoted apoptosis in colorectal cancer cells whereas depletion of NDRG1 resulted in resistance to oxaliplatin treatment.
HCV coopts the MYC pathway responsible for NDRG1 expression and phosphorylation that regulates lipid droplet formation and metabolism. NDRG1 appears to restrict HCV by suppressing the lipid droplet formation that is necessary for HCV assembly.
these data show that NDRG1 is regulated by the oncogenic MAP kinase (Montrer MAPK1 Kits ELISA)-interacting kinase pathway, a target for cancer therapy
The research findings provide novel insights suggesting that loss of N-myc downregulated gene 1 (NDRG1) leads to a decrease in actin-mediated cellular motility but an increase in cellular invasion, resulting in increased tumor dissemination which positively impacts metastatic outcome.
Our experiments revealed that long-term (24 h), but not short-term hypoxia led to the induction of NDRG1 expression in human glioma cell lines. NDRG1 expression was found to correlate with the protein expression of HIF-1alpha (Montrer HIF1A Kits ELISA), SP1 (Montrer PSG1 Kits ELISA), CEBPalpha, YB-1 (Montrer YBX1 Kits ELISA) and Smad7 (Montrer SMAD7 Kits ELISA)
Data show that LSD1 affects motility and invasiveness of neuroblastoma cells by modulating the transcription of the metastasis suppressor NDRG1. Mechanistically, results found that LSD1 co-localizes with MYCN at the promoter region of the NDRG1 gene and inhibits its expression.
Compared with the normal term pregnancies, the expression of both NDRG1 mRNA and protein were significantly high in placentas from preeclampsia, and the expression of NDRG1 in early-onset preeclampsia was higher than that in late-onset preeclampsia.
we demonstrated that the novel molecule of cell migration and invasion, caveolin-1, has direct interaction with NDRG1 in human colorectal cancer cells
strong NDRG1 expression in ciliated epithelial cells in nasal tissues sampled from patients with chronic rhinosinusitis. NDRG1 gene knockdown decreased the transepithelial electrical resistance and increased the dextran permeability. NDRG1 knockdown disrupted tight junctions of airway epithelial cells. NDRG1 knockdown significantly decreased only claudin-9 (Montrer CLDN9 Kits ELISA) expression, but did not decrease other claudin family molecules.
Study elucidates a mechanism of NDRG1-regulated Wnt (Montrer WNT2 Kits ELISA) pathway activation and EMT (Montrer ITK Kits ELISA) via affecting TLE2 (Montrer TLE2 Kits ELISA) and beta-catenin (Montrer CTNNB1 Kits ELISA) expression in esophageal cancer cells.
NDR1 interacts with TRAF3 and interferes with the association of TRAF3 and IL-17R, resulting in increased formation of the activation complex IL-17R-Act1, which is required for the downstream signaling and production of pro-inflammatory factors
NDR1 kinase, activated by the Rap1 (Montrer TERF2IP Kits ELISA) signaling cascade through RAPL and Mst1 (Montrer MST1 Kits ELISA)/Mst2, associated with and recruited kindlin-3 (Montrer FERMT3 Kits ELISA) to the immunological synapses, which was required for high-affinity LFA-1 (Montrer ITGAL Kits ELISA)/ICAM-1 (Montrer ICAM1 Kits ELISA) binding.
Snell, GHKRO, and PAPPA (Montrer PAPPA Kits ELISA)-KO mice express high levels of two proteins involved in DNA repair, O-6-methylguanine-DNA methyltransferase (MGMT (Montrer MGMT Kits ELISA)) and N-myc downstream-regulated gene 1 (NDRG1).
NDRG1 deficiency attenuates the differentiation of macrophage lineage cells, suppressing bone remodeling and inflammatory angiogenesis. This study strongly suggests the crucial role of NDRG1 in differentiation process for macrophages.
Using double knockout of NDR1 and 2 shows that NDRs acted downstream of MST1 (Montrer MST1 Kits ELISA) to mediate the egress of mature thymocytes from the thymus, as well as the interstitial migration of naive T cells within popliteal lymph nodes.
Ndrg1 is phosphorylated and degraded by CD28 (Montrer CD28 Kits ELISA) signalling in a proteasome-dependent manner.
Ndr1/2-double null embryos show defects in somitogenesis and cardiac looping, which reveals their essential functions and shows that the NDR kinases are critically required during the early phase of organogenesis
Rassf5 and Ndr1 or Ndr2 kinases regulate neuronal polarity through Par3 (Montrer F2RL2 Kits ELISA) phosphorylation.
NDRG1 promotes fetal growth and regulates the metabolic response to intrauterine hypoxic injury in a sexually dichotomous manner
early growth response 1 (Montrer EGR1 Kits ELISA), a transcription factor that binds to the NDRG1 promoter, was mediated in the NDRG1 expression regulation by PKD2 (Montrer PKD2 Kits ELISA).
NDR1 plays a broad role both in mediating primary cellular functions in Arabidopsis through maintaining the integrity of the cell wall-plasma membrane connection and as a key signaling component of these responses during pathogen infection.
SR1 plays an important role in plant immunity and ethylene signaling by directly regulating NDR1 and EIN3.
The induction of defence responses and disease resistance to X. campestris pv. campestris strain 8004 requires NDR1 , RAR1 and SGT1b, suggesting that effector-triggered immunity plays a large role in resistance to this strain.
Sequence analysis and mass spectrometry suggest that NDR1 is localized to the PM via a C-terminal glycosylphosphatidyl-inositol (GPI (Montrer GPI Kits ELISA)) anchor.
demonstrate that the RIN4-NDR1 interaction occurs on the cytoplasmically localized N-terminal portion of NDR1 and that this interaction is required for the activation of resistance signaling following infection by P. syringae
Mutations in NDR1 abolished the enhanced resistance of dnd mutants against Pseudomonas syringae pv. tomato and Hyaloperonospora parasitica but not Botrytis cinerea.
This gene is a member of the N-myc downregulated gene family which belongs to the alpha/beta hydrolase superfamily. The protein encoded by this gene is a cytoplasmic protein involved in stress responses, hormone responses, cell growth, and differentiation. The encoded protein is necessary for p53-mediated caspase activation and apoptosis. Mutations in this gene are a cause of Charcot-Marie-Tooth disease type 4D, and expression of this gene may be a prognostic indicator for several types of cancer. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
N-myc downstream-regulated gene 1 protein
, differentiation-related gene 1 protein
, nickel-specific induction protein Cap43
, protein NDRG1
, protein regulated by oxygen-1
, reducing agents and tunicamycin-responsive protein
, N-myc downstream regulated 1
, protein Ndr1
, N-myc downstream regulated gene 1
, protein NDRG1-B
, protein NDRG1-like