scholarly article | Q13442814 |
P50 | author | Anne Joutel | Q47155789 |
Emmanuel Cognat | Q58428999 | ||
Joelle Vinh | Q63806414 | ||
P2093 | author name string | Céline Baron-Menguy | |
Marie Monet-Leprêtre | |||
Iman Haddad | |||
Valérie Domenga-Denier | |||
Meriem Riani | |||
Claire Dussaule | |||
Maï Fouillot-Panchal | |||
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Strong clustering and stereotyped nature of Notch3 mutations in CADASIL patients | Q28255796 | ||
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Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia | Q28294011 | ||
A model for random sampling and estimation of relative protein abundance in shotgun proteomics | Q29547316 | ||
The canonical Notch signaling pathway: unfolding the activation mechanism | Q29547725 | ||
Structure and function of matrix metalloproteinases and TIMPs | Q30014818 | ||
Distinct phenotypic and functional features of CADASIL mutations in the Notch3 ligand binding domain | Q30487788 | ||
Cerebrovascular dysfunction and microcirculation rarefaction precede white matter lesions in a mouse genetic model of cerebral ischemic small vessel disease | Q30492865 | ||
Endothelial-derived PDGF-BB and HB-EGF coordinately regulate pericyte recruitment during vasculogenic tube assembly and stabilization | Q30497541 | ||
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Cadasil | Q33470786 | ||
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Pathogenic mutations associated with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy differently affect Jagged1 binding and Notch3 activity via the RBP/JK signaling Pathway | Q33909665 | ||
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Systemic vascular smooth muscle cell impairment in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy | Q34305487 | ||
Vitronectin in vascular context: facets of a multitalented matricellular protein | Q34631318 | ||
Hypomorphic Notch 3 alleles link Notch signaling to ischemic cerebral small-vessel disease | Q35008186 | ||
Accumulation of tissue inhibitor of metalloproteinases-3 in human eyes with Sorsby's fundus dystrophy or retinitis pigmentosa | Q35303077 | ||
Genetics of ischaemic stroke | Q36713912 | ||
Tissue inhibitors of metalloproteinases in cell signaling: metalloproteinase-independent biological activities. | Q36805538 | ||
Congruence between NOTCH3 mutations and GOM in 131 CADASIL patients | Q37158175 | ||
Amyloid in neurodegenerative diseases: friend or foe? | Q37860535 | ||
Notch signalling in smooth muscle cells during development and disease | Q37977827 | ||
Amyloid-like aggregates sequester numerous metastable proteins with essential cellular functions | Q39610788 | ||
CADASIL mutations enhance spontaneous multimerization of NOTCH3. | Q39856502 | ||
Identification of the extracellular matrix (ECM) binding motifs of tissue inhibitor of metalloproteinases (TIMP)-3 and effective transfer to TIMP-1. | Q40254634 | ||
Notch3 is required for arterial identity and maturation of vascular smooth muscle cells | Q40408474 | ||
Bidirectional encroachment of collagen into the tunica media in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy | Q42013247 | ||
CADASIL-associated Notch3 mutations have differential effects both on ligand binding and ligand-induced Notch3 receptor signaling through RBP-Jk | Q42825763 | ||
Transgenic mice expressing mutant Notch3 develop vascular alterations characteristic of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy | Q42855085 | ||
Evaluation of diagnostic NOTCH3 immunostaining in CADASIL. | Q47900651 | ||
The archetypal R90C CADASIL-NOTCH3 mutation retains NOTCH3 function in vivo | Q48256255 | ||
Expression of drug transporters at the blood-brain barrier using an optimized isolated rat brain microvessel strategy. | Q48323994 | ||
Systemic vascular smooth muscle cell impairment in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy | Q56502592 | ||
Notch3 ectodomain is a major component of granular osmiophilic material (GOM) in CADASIL | Q57187397 | ||
Spectrum of mutations in biopsy-proven CADASIL: implications for diagnostic strategies | Q80357378 | ||
Co-aggregate formation of CADASIL-mutant NOTCH3: a single-particle analysis | Q84235340 | ||
P4510 | describes a project that uses | ImageJ | Q1659584 |
P433 | issue | Pt 6 | |
P407 | language of work or name | English | Q1860 |
P921 | main subject | extracellular matrix | Q193825 |
P304 | page(s) | 1830-1845 | |
P577 | publication date | 2013-05-06 | |
P1433 | published in | Brain | Q897386 |
P1476 | title | Abnormal recruitment of extracellular matrix proteins by excess Notch3 ECD: a new pathomechanism in CADASIL | |
P478 | volume | 136 |
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Q95840655 | Clinical and Genetic Aspects of CADASIL |
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Q37643585 | Endothelial cell-oligodendrocyte interactions in small vessel disease and aging |
Q93102418 | Genetic Factors of Cerebral Small Vessel Disease and Their Potential Clinical Outcome |
Q38433566 | Genetic factors in cerebral small vessel disease and their impact on stroke and dementia |
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Q36417190 | The NOTCH3 score: a pre-clinical CADASIL biomarker in a novel human genomic NOTCH3 transgenic mouse model with early progressive vascular NOTCH3 accumulation |
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Q35175576 | The small leucine-rich proteoglycan BGN accumulates in CADASIL and binds to NOTCH3 |
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