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Two heterozygous missense mutations in the NOTCH3 gene have been identified in two families affected with cerebral autosomal dominant arteriopathy with subcortical infarct and leucoencephalopathy
The results reveal a new connection between p38MAPK (show MAPK14 Proteins), MYC (show MYC Proteins) and NOTCH (show NOTCH1 Proteins) signaling, demonstrate two mechanisms of NOTCH3 regulation and provide evidence for NOTCH3 involvement in prostate luminal cell differentiation.
Results identified NOTCH3 as a direct target of MIR (show MLXIP Proteins)-613 which represses notch3 expression via targeting its 3'TUR. IN contrary, HOTAIR positively regulates the notch3 expression via acting as a competing endogenous RNA for miR (show MLXIP Proteins)-613 binding in pancreatic cancer.
The present study identified a novel variant (chr19:15288426A>C) in the NOTCH3 gene using whole exome sequencing and confirmed it using Sanger sequencing. With multiple in silico analyses and 3D structure simulation, it is suggested that this variant has mildly damaging effects on the function of NOTCH3 gene, but can decrease protein stability.
We find that across species, the atypical receptor NOTCH3 is differentially overexpressed; it is progressively up-regulated with disease development and promotes tumor cell survival via activation of PI3k (show PIK3CA Proteins)-Akt (show AKT1 Proteins)
we report a rare pathogenic mutation on exon 14 of the NOTCH3 gene in a Chinese family affected by CADASIL
The SNPs rs1044009 and rs1044006 in the NOTCH3 gene were associated with the risk of cerebral infarction disease in a Chinese Han agedness population.
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
We find that across species, the atypical receptor NOTCH3 is differentially overexpressed; it is progressively up-regulated with disease development and promotes tumor cell survival via activation of PI3k-Akt (show AKT1 Proteins)
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 Proteins)/3 and promotes transcription of TGFbeta (show TGFB1 Proteins), Smad2 (show SMAD2 Proteins), Smad3 (show SMAD3 Proteins), Notch2 (show NOTCH2 Proteins) and Notch3 which, in turn, results in TGFbeta (show TGFB1 Proteins) and Notch (show NOTCH1 Proteins) pathway activation.
this study shows that Notch (show NOTCH1 Proteins) signaling regulates basophils biological function, at least partially via the modulation of MAPK (show MAPK1 Proteins)
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 Proteins)/Smad3 (show SMAD3 Proteins) signaling.
Data indicate that Notch (show NOTCH1 Proteins) receptors Notch1 (show NOTCH1 Proteins) and Notch3 deficiency compromises pericyte function and contributes to vascular pathologies.
In this study, authors use a smooth muscle-specific (show EIF3K Proteins) deletion of Notch2 (show NOTCH2 Proteins) together with a global Notch3 deletion to produce mice with combinations of mutant and wild-type Notch2 (show NOTCH2 Proteins)/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.
The Notch3 receptor is required earlier within the developing somite to regulate hematopoietic stem cell (HSC (show FUT1 Proteins)) 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 Proteins) gene expression in larvae, and maintains vascular integrity in adults.
new role for Notch (show NOTCH1 Proteins) 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 Proteins)-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