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Oligodendrocytes expressing mutant NOTCH3(R90C) (present in CADASIL disease), exhibited aberrant NOTCH3 proteolytic processing. These cells were less viable and had a higher rate of apoptosis. Cells with NOTCH3(R90C) had higher levels of intrinsic mitochondrial apoptosis, extrinsic death receptor path-related apoptosis, and autophagy compared with cells transfected with wild-type NOTCH3.
Novel variants in NOTCH3 associated with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
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 (show NOTCH4 ELISA Kits)/NICD4 in miR (show MLXIP ELISA Kits)-96- and miR (show MLXIP ELISA Kits)-183-expressing nasopharyngeal carcinoma (NPC (show NPC1 ELISA Kits)) cells suggest the involvement of the NOTCH (show NOTCH1 ELISA Kits) signaling pathway in their tumor suppressive function.
ChIP-seq studies show a high concordance of functional NOTCH1 (show NOTCH1 ELISA Kits) and NOTCH3 genomic binding sites that are enriched in binding motifs for RBPJ (show RBPJ ELISA Kits), the transcription factor that recruits activated Notch (show NOTCH1 ELISA Kits) to DNA. The interchangeability of NOTCH1 (show NOTCH1 ELISA Kits) and NOTCH3 was confirmed by rescue of NOTCH1 (show NOTCH1 ELISA Kits)-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 (show PIN1 ELISA Kits) and Notch3 expression levels, which may further suggest a key role of the newly identified Notch3-Pin1 (show PIN1 ELISA Kits) axis in T-cell Acute Lymphoblastic Leukemia (T-ALL) aggressiveness and progression. Thus, combined suppression of Pin1 (show PIN1 ELISA Kits) and Notch3 proteins may be exploited as an additional target therapy for T-ALL
Data indicate that mRNA high expression level of Notch1 (show NOTCH1 ELISA Kits) 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 (show CYP11A1 ELISA Kits)), HR, and mRNA high expression levels of Notch2 (show NOTCH2 ELISA Kits) and Notch3 were associated with worsen OS for all NSCLC, and mRNA high expression level of Notch4 (show NOTCH4 ELISA Kits) was not found to be associated with to OS for all NSCLC.
Notch3 mutation impairs recovery of cardiac function post-myocardial ischemia.
Notch3 plays an important role in the maintenance of quiescent neural stem cells in the subependymal zone.
Lnc-LFAR1 binds directly to Smad2 (show SMAD2 ELISA Kits)/3 and promotes transcription of TGFbeta (show TGFB1 ELISA Kits), Smad2 (show SMAD2 ELISA Kits), Smad3 (show SMAD3 ELISA Kits), Notch2 (show NOTCH2 ELISA Kits) and Notch3 which, in turn, results in TGFbeta (show TGFB1 ELISA Kits) and Notch (show NOTCH1 ELISA Kits) pathway activation.
this study shows that Notch (show NOTCH1 ELISA Kits) signaling regulates basophils biological function, at least partially via the modulation of MAPK (show MAPK1 ELISA Kits)
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 (show TGFB1 ELISA Kits)/Smad3 (show SMAD3 ELISA Kits) signaling.
Data indicate that Notch (show NOTCH1 ELISA Kits) receptors Notch1 (show NOTCH1 ELISA Kits) and Notch3 deficiency compromises pericyte function and contributes to vascular pathologies.
In this study, authors use a smooth muscle-specific (show EIF3K ELISA Kits) deletion of Notch2 (show NOTCH2 ELISA Kits) together with a global Notch3 deletion to produce mice with combinations of mutant and wild-type Notch2 (show NOTCH2 ELISA Kits)/3 alleles in vascular smooth muscle cells
Elevated levels of TIMP3 (show TIMP3 ELISA Kits) and vitronectin (show VTN ELISA Kits), acting downstream of Notch3(ECD) deposition, play a role in CADASIL, producing divergent influences on early CBF (show CEBPZ ELISA Kits) deficits and later white matter lesions.
Mutant Notch3 accumulates in pericytes and causes progressive pericyte loss and BBB (show ALMS1 ELISA Kits) leakage in the cerebral cortex in CADASIL mouse model.
The Notch3 receptor is required earlier within the developing somite to regulate hematopoietic stem cell (HSC (show FUT1 ELISA Kits)) 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 (show MBP ELISA Kits) gene expression in larvae, and maintains vascular integrity in adults.
new role for Notch (show NOTCH1 ELISA Kits) 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 (show NOTCH1 ELISA Kits)-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