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Mouse (Murine) Notch1 Protein expressed in CHO Cells - ABIN1344230
Fiorini, Merck, Wilson, Ferrero, Jiang, Koch, Auderset, Laurenti, Tacchini-Cottier, Pierres, Radtke, Luther, Macdonald: Dynamic regulation of notch 1 and notch 2 surface expression during T cell development and activation revealed by novel monoclonal antibodies. in Journal of immunology (Baltimore, Md. : 1950) 2009
The rs6563G > A genetic variation appears to be associated with congenital VSD through gene regulatory effects of miR-3691-3p on the NOTCH1 gene.
A critical role for the miR106b-25/NEDD4L/NOTCH1 axis in the disease.
High Notch-1 and low PTEN mRNA expression may predict poorer overall survival.
High NOTCH1 expression is associated with chemoresistance in ovarian cancer.
High Notch1 expression is associated with invasiveness and tumorigenicity of non-small cell lung cancer.
The presence of NOTCH1 mutations might contribute to the disease relapse of T-ALL.
our data link for the first time NOTCH1 mutations to CD49d expression regulation through the involvement of the NF-kappaB pathway in CLL.
The authors found that Notch1 is up-regulated in the wound edge and its expression is dependent on JMJD3 and NF-kappaB in wounded keratinocytes.
The findings indicate that miR-433 may inhibit cell migration and invasion in the development of ovarian cancer via down-regulation of Notch1.
Notch1 siRNA inhibits proliferation and increases apoptosis of hypoxic osteosarcoma cells. Repression of the Notch protein expression resulted in down-regulation of MRP1 protein. These data support the conclusion that Notch1 may represent a viable target to overcome chemoresistant osteosarcoma cells in a hypoxic niche by regulating MRP1 gene expression.
Preliminary data demonstrate a significant association between blood miR-145 expression and the presence of rare NOTCH1 variants. This association may be indicative of a specific pathogenetic pathway in the development of genetically-triggered bicuspid aortopathy and highlights the role of specific miRNAs in the transmission of genetic defects inducing vasculopathy.
the C-terminal region of N1(ICD) plays a role in shaping the Notch response.
Vasorin acts as a switch to augment Notch signaling under hypoxic conditions.
The tumour suppressor role of Notch1 was supported and the use of Notch1 agonists may have a role in improving the prognosis of hepatocellular carcinoma (HCC).
Quantitative single-cell imaging revealed that Dll1 activates Notch1 in discrete, frequency-modulated pulses that specifically upregulate the Notch target gene Hes1. By contrast, Dll4 activates Notch1 in a sustained, amplitude-modulated manner that predominantly upregulates Hey1 and HeyL.
GSK3beta regulates signaling by controlling postendocytic transport of Notch1
these data show an important role for epithelial Notch-1 activation and PLA2-IIA production during health and disease at mucosal surfaces
The frequency of NOTCH1 mutations in 3'UTR region was low. Our findings confirmed current data on the association between the structure of the B-cell receptor and the appearance of NOTCH1 mutations
Findings indicate Notch1 protein (NOTCH1) as a pivotal driver of Group 3 medulloblastoma metastasis and self-renewal, supporting the development of therapies targeting this pathway.
NOTCH1 signaling supports the expression of a subset of inflammatory genes at the enhancer level and key signaling pathways converge on chromatin to coordinate the transition to an inflammatory endothelial phenotype.
Results suggested that Notch1 binds to the promoter region of miR-155, likely repressing its transcription in muscular satellite cells/myoblasts.
Endothelial progenitor cells and Notch-1 signaling are markers of alveolar endothelium regeneration in pulmonary emphysema.
The results of this study suggest that Notch1 plays a vital role in spatial learning and memory, synaptic plasticity under normal physiological conditions and voluntary running conditions.
Hes7 expression in the presomitic mesoderm was up-regulated through the E-box, T-box, and RBPj-binding element in the Hes7 essential region, presumably through synergistic signaling involving mesogenin1, T-box6 (Tbx6), and Notch1.
An additional mechanism by which Notch1 signaling may fine-tune Th1 cell differentiation.
Collectively, these data show that DLL4 preferentially activates NOTCH1 over NOTCH2, whereas DLL1 is equally effective in activating NOTCH1 and NOTCH2, establishing that the ectodomains dictate selective ligand function in vivo, and that features outside the known binding interface contribute to their differences.
Targeting Cadherin-11 Prevents Notch1-Mediated Calcific Aortic Valve Disease.
Notch transduction pathway interferes with outward K(+) Kv currents, critical determinants of the electrical repolarization of myocytes.
Our findings suggest that ischemic stroke in human can also induce angiogenesis in the peri-infarct regions as does in animal models of focal ischemia and that Notch1 signaling plays a critical role in mediating this process
Loss of Wt1 in mature podocytes modulates podocyte Notch activation, which could mediate early events in WT1-related glomerulosclerosis.
The Sox17-Notch1-Hes1 pathway is critical for maintaining the undifferentiated state of IAHCs.
Study provides genetic evidence that Notch1 gain of function in muscles leads to neonatal death and neuromuscular junction (NMJ) formation defects, suggesting Notch1 plays a substantial role in the regulation of myogenesis and NMJ formation. Study demonstrated that Notch1 could regulate AChR gamma to epsilon subunit conversion by direct regulation of the transcription of Chrng genes.
MiR-497 approximately 195 cluster regulates angiogenesis during coupling with osteogenesis by maintaining endothelial Notch1 and HIF1A activity.
These findings suggest that integrin beta1 may be an oxygen-sensitive molecule that promotes keratinocyte migration during wound healing and that Notch1 signaling is involved in this process.
NOTCH1 signalling promotes extracellular matrix (ECM)degradation during the formation of endocardial projections that are critical for individualization of trabecular units, whereas NRG1 promotes myocardial ECM synthesis, which is necessary for trabecular rearrangement and growth.
Structural Divergence in O-GlcNAc Glycans Displayed on Epidermal Growth Factor-like Repeats of Mammalian Notch1.
miR-146b targets to Notch1 and protected cardiomyocytes against inflammation and apoptosis.
It is anegative master modulators of oligodendrocyte differentiation.
Notch initially destabilises beta-catenin in a process that does not depend on its phosphorylation by GSK3
Notch signaling promotes floor plate and hypochord fates over notochord, but has variable effects on Shh expression in the midline.
Transgenic tadpoles were prepared with an elastase promoter driving either the stromelysin-3 gene or the constitutively active form of Notch (IC).
ZFP423 coordinates Notch1 and bone morphogenetic protein signaling, selectively up-regulating Hes5 gene expression.
results suggest that a cell-to-cell interaction via the Notch/Su(H) pathway has a significant role in the PGC migration by regulating cell motility
the process of delimiting the three germ layers requires Notch signaling.
BCL6 inhibits transcription by competing for the Notch1 intracellular domain, preventing the coactivator Mastermind-like1 (MAM1) from binding.
the combination of XSICD-mediated intracellular signaling and the extracellular domain of Notch ligands-mediated activation of Notch receptor is involved in the primary neurogenesis
Notch signaling is activated when activin-like signaling induces various tissues from homogenous undifferentiated cells.
Notch controls smad2 nuclear localization and the competence of ectodermal cells for activin A in Xenopus embryos
Notch signaling has a role during the prepatterning of the cardiac mesoderm
the NOTCH1 polymorphism g.A48250G was significantly associated with body height, body weight, and height at hip cross, and that g.A49239C only showed significant associations with body height
bovine herpesvirus 1 ORF2 protein reduced the trans-activation potential of Notch1 and Notch3, suggesting that ORF2 interfered with the trans-activation potential of Notch.
Cellular size or Notch1 expression is not per se a specific marker for mesenchymal progenitor cells in adult articular cartilage.
This gene encodes a member of the Notch family. Members of this Type 1 transmembrane protein family share structural characteristics including an extracellular domain consisting of multiple epidermal growth factor-like (EGF) repeats, and an intracellular domain consisting of multiple, different domain types. Notch family members play a role in a variety of developmental processes by controlling cell fate decisions. The Notch signaling network is an evolutionarily conserved intercellular signaling pathway which regulates interactions between physically adjacent cells. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signaling pathway that plays a key role in development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remain to be determined. This protein is cleaved in the trans-Golgi network, and presented on the cell surface as a heterodimer. This protein functions as a receptor for membrane bound ligands, and may play multiple roles during development.
, Notch homolog 1, translocation-associated (Drosophila)
, Notch homolog 1, translocation-associated
, neurogenic locus notch homolog protein 1
, translocation-associated notch protein TAN-1
, Motch A
, Notch gene homolog 1
, major type A protein
, transmembrane receptor Notch1
, Drosophila Notch homolog 1 (controlling the the ectodermal and neural cell fate in Drosophila)
, neurogenic locus notch protein homolog