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NOTCH3 single-nucleotide polymorphisms role in susceptibility to non-small cell lung cancer
Single-nucleotide polymorphism in NOTCH3 gene is associated with breast cancers.
Reduced NOTCH3/NICD3 and NOTCH4 (zeige NOTCH4 Proteine)/NICD4 in miR (zeige MLXIP Proteine)-96- and miR (zeige MLXIP Proteine)-183-expressing nasopharyngeal carcinoma (NPC (zeige NPC1 Proteine)) cells suggest the involvement of the NOTCH (zeige NOTCH1 Proteine) signaling pathway in their tumor suppressive function.
ChIP-seq studies show a high concordance of functional NOTCH1 (zeige NOTCH1 Proteine) and NOTCH3 genomic binding sites that are enriched in binding motifs for RBPJ (zeige RBPJ Proteine), the transcription factor that recruits activated Notch (zeige NOTCH1 Proteine) to DNA. The interchangeability of NOTCH1 (zeige NOTCH1 Proteine) and NOTCH3 was confirmed by rescue of NOTCH1 (zeige NOTCH1 Proteine)-dependent T-ALL cells with activated NOTCH3 and vice versa.
Low Notch3 expression is associated with left ventricle hypertrabeculation/non-compaction and Menetrier-like gastropathy.
High NOTCH3 expression is associated with basal breast cancer.
in in silico gene expression analysis of human T-ALL samples we observed a significant correlation between Pin1 (zeige PIN1 Proteine) and Notch3 expression levels, which may further suggest a key role of the newly identified Notch3-Pin1 (zeige PIN1 Proteine) axis in T-cell Acute Lymphoblastic Leukemia (T-ALL) aggressiveness and progression. Thus, combined suppression of Pin1 (zeige PIN1 Proteine) and Notch3 proteins may be exploited as an additional target therapy for T-ALL
Data indicate that mRNA high expression level of Notch1 (zeige NOTCH1 Proteine) was associated with better overall survival (OS) for all NSCLC, hazard ratio (HR), better OS in adenocarcinoma (Ade), HR, as well as in squamous cell carcinoma (SCC (zeige CYP11A1 Proteine)), HR, and mRNA high expression levels of Notch2 (zeige NOTCH2 Proteine) and Notch3 were associated with worsen OS for all NSCLC, and mRNA high expression level of Notch4 (zeige NOTCH4 Proteine) was not found to be associated with to OS for all NSCLC.
MicroRNA-136 inhibits cancer stem cell activity and enhances the anti-tumor effect of paclitaxel against chemoresistant ovarian cancer cells by targeting Notch3 pathway.
Intermittent compressive stress regulates Notch (zeige NOTCH1 Proteine) receptor and target gene expression via the TGF-beta (zeige TGFB1 Proteine) signaling pathway. Notch (zeige NOTCH1 Proteine) signaling participates in TGF-beta (zeige TGFB1 Proteine)-induced sclerostin (zeige SOST Proteine) expression in periodontal ligament cells.
Lnc-LFAR1 binds directly to Smad2 (zeige SMAD2 Proteine)/3 and promotes transcription of TGFbeta (zeige TGFB1 Proteine), Smad2 (zeige SMAD2 Proteine), Smad3 (zeige SMAD3 Proteine), Notch2 (zeige NOTCH2 Proteine) and Notch3 which, in turn, results in TGFbeta (zeige TGFB1 Proteine) and Notch (zeige NOTCH1 Proteine) pathway activation.
this study shows that Notch (zeige NOTCH1 Proteine) signaling regulates basophils biological function, at least partially via the modulation of MAPK (zeige MAPK1 Proteine)
Knock-in mice with the R169C mutation (Notch3(R170C/R170C)) exhibited similar reductions in arterial lumen, and both TgNotch3(R169C) and Notch3(R170C/R170C) mice showed increased cerebral artery expression of Notch3 target genes.
Notch3 is an important protective factor for cardiac fibrosis in a myocardial infarction model, and the protective effect of Notch3 is attributable to its action on TGF-beta1 (zeige TGFB1 Proteine)/Smad3 (zeige SMAD3 Proteine) signaling.
Data indicate that Notch (zeige NOTCH1 Proteine) receptors Notch1 (zeige NOTCH1 Proteine) and Notch3 deficiency compromises pericyte function and contributes to vascular pathologies.
In this study, authors use a smooth muscle-specific (zeige EIF3K Proteine) deletion of Notch2 (zeige NOTCH2 Proteine) together with a global Notch3 deletion to produce mice with combinations of mutant and wild-type Notch2 (zeige NOTCH2 Proteine)/3 alleles in vascular smooth muscle cells
Elevated levels of TIMP3 and vitronectin, acting downstream of Notch3(ECD) deposition, play a role in CADASIL, producing divergent influences on early CBF deficits and later white matter lesions.
Mutant Notch3 accumulates in pericytes and causes progressive pericyte loss and BBB leakage in the cerebral cortex in CADASIL mouse model.
Relative to air-exposed controls, ozone increased bronchoalveolar lavage fluid protein, a marker of lung permeability, in all genotypes, but significantly greater concentrations were found in Notch4 (zeige NOTCH4 Proteine)-/- compared with wild-type and Notch3-/- mice.
The mechanism of Oncostatin M (zeige OSM Proteine) on cardiac ischemia/reperfusion injury is partly mediated by the Notch3/Akt (zeige AKT1 Proteine) pathway.
The Notch3 receptor is required earlier within the developing somite to regulate hematopoietic stem cell (HSC (zeige FUT1 Proteine)) emergence in a non-cell-autonomous manner.
90 % of proliferating radial glia express notch1a, notch1b and notch3. In contrast, the proliferating non-glial populations of the dorsal telencephalon and hypothalamus rarely express notch3 and about half express notch1a/1b.
Notch3 regulates oligodendrocyte precursor cells development and mbp (zeige MBP Proteine) gene expression in larvae, and maintains vascular integrity in adults.
new role for Notch (zeige NOTCH1 Proteine) signaling in brain vascular development whereby Notch3 signaling promotes expansion of the brain pericyte population
Notch3 activity gates neural stem cell activation in the adult pallium.
Cellular correlates of Notch (zeige NOTCH1 Proteine)-delta gene expression in the regenerating zebrafish retina.
knockdown of notch3 function in notch1a mutants leads to the loss of rhombomere boundary cells and causes neuronal hyperplasia
This gene encodes the third discovered human homologue of the Drosophilia melanogaster type I membrane protein notch. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signalling pathway that plays a key role in neural development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remains to be determined. Mutations in NOTCH3 have been identified as the underlying cause of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
Notch homolog 3
, neurogenic locus notch homolog protein 3
, Notch gene homolog 3