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The rs3815188 variant and rs1043994 variant of the Notch3 gene is associated with lung cancer risk in patients of Turkish origin.
Case Report: mutation p.Cys212Gly in 1 allele of the NOTCH-3 gene in mother/daughter with CADASIL.
Notch3 rs3815188, DLL1 rs1033583, JAG1 rs8708, JAG2 rs9972231, HEY1 rs1046472, HEY2 rs3734637 and HES2 rs11364 were significantly associated with susceptibility to lung cancer.
These results connect HDAC6 activity to regulation of total and surface Notch3 levels.
Importantly, deregulated Notch3 expression and/or activation, often results in disrupted cell differentiation and/or pathological development, most notably in oncogenesis in different cell contexts. Mechanistically this is due to Notch3-related genetic alterations or epigenetic or posttranslational control mechanisms.
Results reveal that CAF-induced expression of Notch3 is responsible for LSD1 activation in CSC, driving their self-renewal in HCC. These seminal findings illuminate a complex pathway in the tissue microenvironment of liver cancer, which is responsible for orchestrating the self-renewal of stem-like cancer cells.
higher JAG1 expression was found in MCPyV-negative than in MCPyV-positive MCC (p<0.001), and NOTCH3 expression was higher in MCPyV-positive MCC (p=0.062). Kaplan-Meier and multivariate analyses showed that patients with MCC with higher NOTCH3 expression had better overall survival than otherwise (p=0.001 and p=0.033, respectively).
novel exon 8 mutation (c.1337G>A; p.Cys446Tyr) in NOTCH3 gene is associated with CADASIL (Cerebral Arteriopathy with Subcortical Infarcts and Leukoencephalopathy).
aberrantly expressed in the pathological tumour vascularization where it limits tumour angiogenesis through a pro-apoptotic activity
TGFbeta activates the transcription factor ZEB1 to repress Notch3, thereby limiting terminal differentiation.
A novel NOTCH3 pathogenic variant (p.N1969 *) in the intracellular ankyrin repeat domain is detected in three CADASIL patients.
TNFalpha regulates NOTCH2 and NOTCH3 expression in pulmonary artery smooth muscle cells via preferential ACTR-IIA signalling in BMPR-II-deficient cells.
SIRT6 may suppress cell proliferation, migration, and invasion via inhibition of the NOTCH3 signaling pathway in glioma
hus Notch3 appears to be a promising target for gene therapy and DAPT is able to mediate a strong antitumor effect in nonsmall cell lung cancer (NSCLC) cells that overexpress Notch3. Further studies of a combined treatment regimen with DAPT and GEM are warranted and may provide greater efficacy and safety in the treatment of NSCLC patients
Adult-onset Mendelian leukodystrophy genes are not common factors implicated in Alzheimer's disease, but there is a potential pathogenic link between NOTCH3, CSF1R, and sporadic late-onset Alzheimer's disease.
Vascular smooth muscle cells were cyclically stretched on flexible membranes. Expression of Jagged1, Notch3, and target genes was down-regulated with strain. Upon increasing thickness, the model predicted a switch-type behavior of Notch signaling state with a steep transition of synthetic toward contractile VSMCs at a certain thickness. The Notch response to hemodynamics plays an important role in vascular homeostasis.
A threshold level of NFATc1 activity facilitates thymocyte differentiation and opposes Notch3-driven leukemia development.
We describe a CADASIL family with a novel R110C mutation in the NOTCH3 gene
The levels of markers related to PaSC activation, such as a-smooth muscle actin (alpha-SMA), collagen I and fibronectin, decreased in response to Notch3 knockdown, indicating that Notch3 plays an important role in PaSC activation. Furthermore, we confirmed that inhibition of PaSC activation via Notch3 siRNA reduced the proliferation and migration of PaSC-induced mouse pancreatic cancer (LTPA) cells.
The novel variant c.128G>C in exon 2 of NOTCH3 was identified in 2 patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
our results provide direct evidences that miR-206 regulates skeletal muscle cells proliferation and cell cycle arrest partly by targeting the Notch3 gene, which strengthens our understanding of regulatory mechanisms on miR-206 in skeletal muscle growth and development.
The Notch3(tm1.1Ecan) mutation was introduced into mice, and it was found that this mutation causes osteopenia despite an increase in osteoblast proliferation and function and is associated with enhanced Tnfsf11 expression in osteoblasts and osteocytes.
endothelial expression of Notch3 limits tumour angiogenesis; tumour growth and angiogenesis are increased when Notch3 is silenced in the stroma
Double immunostaining with differentiation markers revealed that NOTCH3 was expressed in some undifferentiated and differentiated spermatogonia in mouse testes.
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
overexpression demonstrates an antiproliferative effect on established metastatic medullary thyroid cancer liver tumors
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 Smad2/3 and promotes transcription of TGFbeta, Smad2, Smad3, Notch2 and Notch3 which, in turn, results in TGFbeta and Notch pathway activation.
this study shows that Notch signaling regulates basophils biological function, at least partially via the modulation of MAPK
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/Smad3 signaling.
Data indicate that Notch receptors Notch1 and Notch3 deficiency compromises pericyte function and contributes to vascular pathologies.
In this study, authors use a smooth muscle-specific deletion of Notch2 together with a global Notch3 deletion to produce mice with combinations of mutant and wild-type Notch2/3 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-/- compared with wild-type and Notch3-/- mice.
The mechanism of Oncostatin M on cardiac ischemia/reperfusion injury is partly mediated by the Notch3/Akt pathway.
miR-7a regulates the differentiation of Muller glia through the suppression of Notch3 expression.
Study showed Notch3 expressed in proliferating hippocampal precursor cells and down-regulates their activation and proliferation; adult neurogenesis in CADASIL transgenic mice was altered prior to vascular abnormalities due to deficits in Notch3 signaling
The results demonstrate that quiescence and stemness are molecularly distinct outputs of Notch3 signalling, and identify Hey1 as a major Notch3 effector controlling NSC stemness in the vertebrate adult brain.
The Notch3 receptor is required earlier within the developing somite to regulate hematopoietic stem cell (HSC) 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 gene expression in larvae, and maintains vascular integrity in adults.
new role for Notch 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-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