Results 61 to 70 of about 17,508 (213)

The association between NOTCH3 expression and the clinical outcome in the urothelial bladder cancer patients

open access: yesBiomolecules & Biomedicine, 2022
Disrupted NOTCH activity is a driving event in urothelial bladder cancer (UBC). After activation by hypoxia, the NOTCH3 receptor participates in tumor cell proliferation, acquisition of the epithelial-mesenchymal transition phenotype, and angiogenesis ...
Ana Ristic Petrovic   +7 more
doaj   +1 more source

A transition zone enriched WIF1+ basal cell subtype is associated with benign prostatic hyperplasia

open access: yesThe Journal of Pathology, EarlyView.
Abstract The cellular composition and disease susceptibilities of the distinct zones of the human prostate remain incompletely understood. Benign prostatic hyperplasia (BPH) is a common condition that causes widespread morbidity and is nearly exclusively localized to the transition zone (TZ).
Rulin Wang   +20 more
wiley   +1 more source

Investigation of the NOTCH3 and TNFSF7 Genes on C19p13 as Candidates for Migraine [PDF]

open access: yes, 2008
To investigate the migraine locus around the C19p13 region through analysis of the NOTCH3 gene (C19p13.2- p13.1), previously shown to be a gene involved in CADASIL and the TNFSF7 gene (C19p13), homologous to the ligands of TNF-alpha and TNF-beta, genes
Mick Ovcaric   +16 more
core   +2 more sources

A NOTCH3 pathogenic variant influences osteogenesis and can be targeted by antisense oligonucleotides in induced pluripotent stem cells.

open access: yesPLoS ONE
Lateral Meningocele Syndrome (LMS), a disorder associated with NOTCH3 pathogenic variants, presents with neurological, craniofacial and skeletal abnormalities.
Ernesto Canalis   +4 more
doaj   +1 more source

PPM1G‒MET axis sustains AKT signaling to drive Twist‐associated EMT and drug resistance in hepatocellular carcinoma

open access: yesVIEW, EarlyView.
Hepatocellular carcinoma (HCC) is frequently resistant to targeted therapies. We identify protein phosphatase Mg2+/Mn2+‐dependent 1G (PPM1G) as a key phosphatase that stabilizes mesenchymal‐epithelial transition factor (MET) by inhibiting its ubiquitination, thereby sustaining protein kinase B (AKT) signaling and promoting Twist‐mediated epithelial ...
Weixun Wu   +8 more
wiley   +1 more source

Extracellular domain shedding of NOTCH3 during endocytosis associated with heterogeneity between different CADASIL mutant activation mechanisms

open access: yesCell Communication and Signaling
Background Mutations in NOTCH3 cause CADASIL, a dominantly inherited condition, linked to recurrent stroke and vascular dementia and associated with accumulation of the ECD of NOTCH3. The latter has a toxic effect on VSMCs.
Samira Hosseini-Alghaderi, Martin Baron
doaj   +1 more source

Association of NOTCH3 Gene Polymorphisms with Ischemic Stroke and Its Subtypes: A Meta-Analysis

open access: yesMedicina, 2019
Background and objectives: NOTCH3 gene variations play a significant role in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
Loo Keat Wei   +3 more
doaj   +1 more source

Identification of Copy Number Variants as a Suspected Cause of Cerebral Small Vessel Disease

open access: yesClinical Genetics, EarlyView.
Whole‐exome sequencing of 111 patients with suspected familial cerebral small vessel disease (CSVD) identified novel copy number variants in four patients across NOTCH3, LMNB1, and COL4A2, using bioinformatic and molecular techniques. These validated CNVs suggest structural variation is an underrecognized potential causal contributor to monogenic CSVD ...
Solomon K. Guyler   +5 more
wiley   +1 more source

NOTCH3 alterations analysis in malignant glioma samples.

open access: yes, 2013
(A) NOTCH3 gene expression in representative specimens using quantitative-real time PCR showing high levels of NOTCH3 transcripts in various tumor specimens compared to non-tumor samples (epilepsy biopsies; CNTR).
Timothy C. Ryken (413028)   +5 more
core   +1 more source

N3ICD with the transmembrane domain can effectively inhibit EMT by correcting the position of tight/adherens junctions

open access: yesCell Adhesion & Migration, 2019
EMT allows a polarized epithelium to lose epithelial integrity and acquire mesenchymal characteristics. Previously, we found that overexpression of the intracellular domain of Notch3 (N3ICD) can inhibit EMT in breast cancer cells. In this study, we aimed
Junyu Tan   +7 more
doaj   +1 more source

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