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that NOTCH4 expression was decreased in colorectal cancer
Results suggest NOTCH4 SNPs as possible genetic risk factors for the development and clinical presentation of brain arteriovenous malformation and a role of NOTCH4 in the pathogenesis of this disease.
In HNSCC, the NOTCH4-HEY1 pathway is specifically upregulated, induces proliferation and cisplatin resistance, and promotes EMT.
NOTCH4 expression was negatively controlled by RUNX1 via a novel regulatory DNA element within the locus, and this work examined its involvement in megakaryocyte generation. Specific inactivation of NOTCH4 by an improved CRISPR-Cas9 system in human induced pluripotent stem cells enhanced megakaryopoiesis.
NOTCH4 is highly expressed in oral squamous cell carcinoma lesions, but downregulated in oral verrucous carcinoma compared with normal tissue.
Results provide evidence that Notch4 plays an important role in vasculogenic mimicry formation and tumor invasion in hepatocellular carcinoma.
The results of the present study show that RNA interference targeting against Notch-4 expression suppresses prostate cancer progression.
Sirt6 inhibits Notch1 and Notch4 transcription by deacetylating histone H3K9.
Very rare missense variant in the regulatory NODP domain of NOTCH4 located at the 6p21 locus was identified in a single family.This family suggests a novel mechanism of systemic sclerosis pathogenesis in which a rare and penetrant coding variation can substantially elevate disease risk in contrast to the more modest non-coding variation typically found at this locus.
High NOTCH4 expression is associated with preeclampsia.
Reduced NOTCH3/NICD3 and NOTCH4/NICD4 in miR-96- and miR-183-expressing nasopharyngeal carcinoma (NPC) cells suggest the involvement of the NOTCH signaling pathway in their tumor suppressive function.
Data indicate that mRNA high expression level of Notch1 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), HR, and mRNA high expression levels of Notch2 and Notch3 were associated with worsen OS for all NSCLC, and mRNA high expression level of Notch4 was not found to be associated with to OS for all NSCLC.
Low levels of Notch pathway genes Notch1, Notch2, Notch4 and Jagged1 correlated with poor prognostic factors such as larger tumor size, positive lymph-node status, tumor phenotype and infiltrating tumor Treg cells.
Data suggest that the vascular DLL4-Notch4 signaling and VEGF signaling complementing each other plays an important role in the progression of tumor angiogenesis in primary glioblastoma.
findings indicate that Notch4+ melanoma cancer stem-like cells trigger epithelial-mesenchymal transition and promote the metastasis of melanoma cells
the aberrant activation of Notch4 promotes oral squamous cell carcinoma metastasis.
data are consistent with those obtained in previous studies that suggested that rs204993 is associated with schizophrenia and that the AA genotype of rs204993 demonstrates a higher risk
High Notch4 expression is associated with Prostatic Intraepithelial Neoplasia.
The expression of cytoplasmic Notch1 or nuclear Notch4 could also be upregulated by HBx in HepG2X cells. The upregulation of Notch1 by HBx was through p38 MAPK pathway.
Anti-estrogen resistance in human breast tumors is driven by JAG1-NOTCH4-dependent cancer stem cell activity.
Jag1 on alveolar macrophages interacts with Notch 4 on naive allergen-specific T cells to promote TH2 and TH17 cell differentiation
Notch4 inhibited Mycobacterium tuberculosis-induced production of proinflammatory cytokines by interaction with TAK1 and inhibition of its activation.
Int3 activates NF-kappaB in HC11 cells in absence of Rbpj through an association with the IKK signalosome. Int3 induced the canonical NF-kappaB activity and P50 phosphorylation in HC11 cells without altering the NF-kappaB2 pathway. The minimal domain within the Int3 protein required to activate NF-kappaB consists of the CDC10/Ankyrin (ANK) repeats domain.
this study shows that Notch signaling regulates basophils biological function, at least partially via the modulation of MAPK
Report impaired Notch4 signaling in endothelial progenitor cells isolated from mouse Kawasaki disease model.
Notch4-knock-out mice that also lacked Notch1, had defects in all vascular beds.
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.
Constitutively active Notch4 receptor elicits brain arteriovenous malformations through enlargement of capillary-like vessels.
Notch signaling is required for proper lymphatic valve formation and regulates integrin alpha9 and fibronectin EIIIA expression during valve morphogenesis
Notch4-deficient mice exhibited slightly delayed vessel growth in the retina, consistent with the novel finding that NOTCH4 protein is expressed in the newly formed vasculature.
Data indicate that expression of Dll4 is specific to theca layer endothelial cells (ECs); Notch1/Notch4 in theca layer ECs and vascular smooth muscle cells (VSMCs), Notch3 is restricted to VSMCs; Notch2 in granulosa cells (GCs) of small follicles.
In this study, we examined Notch signaling in the well established Tg26 mouse model of HIV associated nephropathy.
Notch4 normalization reduces blood vessel size in arteriovenous malformations
results demonstrate that whey acidic protein promoter-Int3 has no oncogenic effect upon parity-identified mammary epithelial cells
Trp53 regulates Notch 4 signaling through physical interactions with Mdm2.
Results indicate the importance of Notch signaling in maintaining the lung vasculature and offer a new, reliable model with which to study the pathobiology of lung arteriovenous shunts and malformations.
PBP is essential for the growth of Notch4-immortalized mammary cells by activating SOX10 expression, providing a potential molecular mechanism through which PBP regulates the growth of mammary stem/progenitor cells.
Expression of activated Notch1 or Notch4 in endothelial cells causes transdifferentiation to a mesenchymal phenotype. Notch 4 is expressed in the ventricular outflow tract during stages of endocardial cushion formation.
Mice carrying a R142C Notch4 knock-in mutation do not develop a CADSIL phenotype.
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 a role in vascular, renal and hepatic development. This gene may be associated with susceptibility to schizophrenia in a small portion of cases. An alternative splice variant has been described but its biological nature has not been determined.
Notch homolog 4
, neurogenic locus notch homolog protein 4
, notch 4
, neurogenic locus notch homolog protein 4-like
, Notch gene homolog 4
, putative Notch4 protein