Results 41 to 50 of about 2,529,505 (194)

Pathological changes and molecular ⁃ genetic mechanisms of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

open access: yesChinese Journal of Contemporary Neurology and Neurosurgery, 2021
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a inherited cerebral small vessel disease caused by Notch3 gene mutation. The molecular⁃genetic mechanisms of CADASIL have been still unclear.
SUN Yuan⁃jing, FAN Yu⁃hua
doaj   +1 more source

NOTCH3-positive CAFs promotes angiogenesis.

open access: yes, 2016
A and B: Comparison of the microvessel density (MVD) between NOTCH3(-) CAFs and NOTCH3(+)CAFs cases. Immunofluorostaining for α-SMA (green), NOTCH3 (green) and CD34 (red) using human tongue OSCC samples. Ca, cancer nests.
Takumi Akashi (528834)   +11 more
core   +1 more source

Silencing of NOTCH3 Signaling in Meniscus Smooth Muscle Cells Inhibits Fibrosis and Exacerbates Degeneration in a HEYL‐Dependent Manner

open access: yesAdvanced Science, 2023
The mechanisms of meniscus fibrosis and novel ways to enhance fibrosis is unclear. This work reveals human meniscus fibrosis initiated at E24 weeks. Smooth muscle cell cluster is identified in embryonic meniscus, and the combined analysis with previous ...
Hao Sun   +7 more
doaj   +1 more source

The expression of ASAP3 and NOTCH3 and the clinicopathological characteristics of adult glioma patients

open access: yesOpen Medicine, 2022
ASAP3 is involved in a variety of biological activities, including cancer progression in humans. In adult glioma, we explore the effects of ASAP3 and NOTCH3 and their relationships on prognosis.
Su Li-ping   +7 more
doaj   +1 more source

Identification of a known mutation in Notch 3 in familiar CADASIL in China. [PDF]

open access: yesPLoS ONE, 2012
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited disease leading to recurrent ischemic stroke and vascular dementia.
Zhen-Xuan Tan   +7 more
doaj   +1 more source

Notch signaling pathway in human vascular smooth muscle cell differentiation [PDF]

open access: yes, 2006
Notch receptor-ligand interactions are a highly conserved mechanism, originally described in developmental studies using Drosophilae, that regulate inter-cell communication and dictate, in part, vascular smooth muscle cell (VSMC) fate in response to ...
Scheller, Agnieszka
core   +2 more sources

Investigating diagnostic sequencing techniques for CADASIL diagnosis

open access: yesHuman Genomics, 2020
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a cerebral small vessel disease caused by mutations in the NOTCH3 gene.
P. J. Dunn   +5 more
doaj   +1 more source

The infantile myofibromatosis NOTCH3 L1519P mutation leads to hyperactivated ligand-independent Notch signaling and increased PDGFRB expression

open access: yesDisease Models & Mechanisms, 2021
Infantile myofibromatosis (IMF) is a benign tumor form characterized by the development of nonmetastatic tumors in skin, bone, muscle and sometimes viscera. Autosomal-dominant forms of IMF are caused by mutations in the PDGFRB gene, but a family carrying
Dan Wu   +10 more
doaj   +1 more source

Cyclic Mechanical Loading of Cardiomyocytes via Pressure‐Driven Non‐Planar Membrane Deformation in a Bioreactor System

open access: yesAdvanced Science, EarlyView.
In this research article, Mansoor and coworkers present a novel device that applies controlled mechanical stimuli to cardiomyocytes using pressure‐driven membrane deformation. By exposing cells to physiologically and pathologically relevant loading conditions, the platform reproduces distinct structural, functional and molecular responses associated ...
Haris Mansoor   +11 more
wiley   +1 more source

Surfaceome Reprogramming of Stemsomes Promotes Lung Cancer Targeting via Potentiated Receptor–Ligand Interactions

open access: yesAdvanced Science, EarlyView.
This study presents a surfaceome‐reprogramming strategy for mutation‐independent lung cancer therapy by repurposing dexamethasone to prime mesenchymal stem cell‐derived nanovesicles. The engineered vesicles leverage multi‐valent interactions mediated by upregulated adhesion proteins, EPHA2, and NOTCH3.
Geunhye Kim   +8 more
wiley   +1 more source

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