Results 11 to 20 of about 23,019 (220)

Notch3 in Development, Health and Disease [PDF]

open access: yesBiomolecules, 2020
Notch3 is one of four mammalian Notch proteins, which act as signalling receptors to control cell fate in many developmental and adult tissue contexts.
Samira Hosseini Alghaderi, Martin Baron
exaly   +7 more sources

Notch3 interactome analysis identified WWP2 as a negative regulator of Notch3 signaling in ovarian cancer. [PDF]

open access: yesPLoS Genetics, 2014
The Notch3 signaling pathway is thought to play a critical role in cancer development, as evidenced by the Notch3 amplification and rearrangement observed in human cancers.
Jin-Gyoung Jung   +7 more
doaj   +4 more sources

Reduced SUMOylation impairs NOTCH3 signaling and cell survival in the pathogenesis of CADASIL [PDF]

open access: yesCell Communication and Signaling
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebral small vessel disease caused by NOTCH3 mutation.
Lijun Long   +5 more
doaj   +2 more sources

Notch3 and the Notch3-upregulated RNA-binding protein HuD regulate Ikaros alternative splicing [PDF]

open access: yesEMBO Journal, 2007
Constitutive activation of the transmembrane receptor, Notch3, and loss of function of the hematopoietic transcription repressor, Ikaros (IK), play direct roles in T-cell differentiation and leukemogenesis that are dependent on pre-T-cell receptor (pre-TCR) signaling.
Diana Bellavia   +2 more
exaly   +4 more sources

Necessity of Notch3 signaling in myofiber maturation in a pluripotent stem cell transplant model [PDF]

open access: yesSkeletal Muscle
Background Pluripotent stem cell-derived myogenic progenitors change from an embryonic to a postnatal molecular signature upon engrafting as satellite cells, which coincides with upregulation of Notch3.
Aline M. S. Yamashita   +10 more
doaj   +2 more sources

The NOTCH3 score: a pre-clinical CADASIL biomarker in a novel human genomic transgenic mouse model with early progressive vascular NOTCH3 accumulation [PDF]

open access: yesActa Neuropathologica Communications, 2015
CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) is a hereditary small vessel disease caused by mutations in the NOTCH3 gene, leading to toxic NOTCH3 protein accumulation in the small- to medium sized arterioles.
Rutten, J.W.   +12 more
core   +5 more sources

Use of antisense oligonucleotides to target Notch3 in skeletal cells.

open access: yesPLoS ONE, 2022
Notch receptors are determinants of cell fate and function, and play an important role in the regulation of bone development and skeletal remodeling. Lateral Meningocele Syndrome (LMS) is a monogenic disorder associated with NOTCH3 pathogenic variants ...
Ernesto Canalis   +4 more
doaj   +2 more sources

Detection of Vascular Notch3 Deposits in Unfixed Frozen Skin Biopsy Sample in CADASIL

open access: yesFrontiers in Neurology, 2022
This study aimed to evaluate the utility of immunohistochemical staining of vascular Notch3 deposits in biopsied unfixed frozen skin samples from patients with suspected cerebral autosomal dominant arteriopathy with subcortical infarcts and ...
Akihiko Ueda   +8 more
doaj   +1 more source

Biochemical characterization and cellular effects of CADASIL mutants of NOTCH3. [PDF]

open access: yesPLoS ONE, 2012
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is the best understood cause of dominantly inherited stroke and results from NOTCH3 mutations that lead to NOTCH3 protein accumulation and selective ...
He Meng   +6 more
doaj   +1 more source

The archetypal R90C CADASIL–NOTCH3 mutation retains NOTCH3 function in vivo [PDF]

open access: yesHuman Molecular Genetics, 2007
Cerebral Autosomal Dominant Arteriopathy with Subcortical infarcts and Leukoencephalopathy (CADASIL) is the most prominent known cause of inherited stroke and vascular dementia in human adult. The disease gene, NOTCH3, encodes a transmembrane receptor primarily expressed in arterial smooth muscle cells (SMC).
Monet, M   +9 more
openaire   +2 more sources

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