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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Notch 3

Notch3, CADASIL, Notch4
This gene encodes the third discovered human homologue of the Drosophilia melanogaster type I membrane protein notch. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signalling pathway that plays a key role in neural development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remains to be determined. Mutations in NOTCH3 have been identified as the underlying cause of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: AGE, HAD, CAN, Aura, p300
Papers using Notch3 antibodies
Gene expression prowles during activation of cultured rat hepatic stellate cells by tumoral hepatocytes and fetal bovine serum
Dupuy Evelyne et al., In Gastroenterology Research and Practice, 2009
... Becton Dickinson, Le Pont de Claix, France); rabbit anti-Notch4, recognizing the truncated intracellular domain of int3/Notch4 (Upstate, Euromedex, Mundolsheim, France and Abcam, Cambridge, UK); goat anti- ...
Papers on Notch3
Lateral meningocele (Lehman) syndrome: A child with a novel NOTCH3 mutation.
Carter et al., Toronto, Canada. In Am J Med Genet A, Feb 2016
Heterozygous NOTCH3 mutations affecting the terminal exon 33 were recently reported as causative in six families with LMS.
ChIP-BIT: Bayesian inference of target genes using a novel joint probabilistic model of ChIP-seq profiles.
Xuan et al., Arlington, United States. In Nucleic Acids Res, Jan 2016
We applied ChIP-BIT to find target genes from NOTCH3 and PBX1 ChIP-seq data acquired from MCF-7 breast cancer cells.
Vascular cognitive impairment: Modeling a critical neurologic disease in vitro and in vivo.
Murphy et al., Lexington, United States. In Biochim Biophys Acta, Jan 2016
This includes in vitro models of the neurovascular unit, models of chronic cerebral hypoperfusion, animals with NOTCH3 mutations as a model of small vessel disease, large animals with cerebral amyloid angiopathy (CAA), and animal models of mixed dementia.
Annals of Neurology: Volume 78, Number 6, December 2015.
In Ann Neurol, Dec 2015
ON THE COVER Notch3 aggregation is one of the important hallmarks of CADASIL.
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) - literature review apropos an autopsy case.
Iżycka-Świeszewska et al., Gdańsk, Poland. In Pol J Pathol, Sep 2015
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a non-atherosclerotic, non-amyloid cerebral angiopathy involving small arteries and arterioles.
Genetic factors in cerebral small vessel disease and their impact on stroke and dementia.
Dichgans et al., München, Germany. In J Cereb Blood Flow Metab, May 2015
Recent findings include a role of structural constituents of the ECM such as type IV collagens in hereditary and sporadic SVD, the sequestration of proteins with a known role in ECM maintenance into aggregates of NOTCH3, and altered signaling through molecules known to interact with the ECM.
Network-assisted analysis of primary Sjögren's syndrome GWAS data in Han Chinese.
Wang et al., Beijing, China. In Sci Rep, 2014
Of these pSS candidates, 14 genes had been reported to be associated with any of pSS, RA, and SLE, including STAT4, GTF2I, HLA-DPB1, HLA-DRB1, PTTG1, HLA-DQB1, MBL2, TAP2, CFLAR, NFKBIE, HLA-DRA, APOM, HLA-DQA2 and NOTCH4.
Knowledge-based analysis of genetic associations of rheumatoid arthritis to inform studies searching for pleiotropic genes: a literature review and network analysis.
Rao et al., Beijing, China. In Arthritis Res Ther, 2014
RESULTS: In total, we extracted 116 potential functional pleiotropic genes for RA and eight other diseases, including five hub pleiotropic genes, BTNL2, HLA-DRA, NOTCH4, TNXB, and C6orf10, where BTNL2, NOTCH4, and C6orf10 are novel pleiotropic genes identified by our analysis.
The NOTCH3 score: a pre-clinical CADASIL biomarker in a novel human genomic NOTCH3 transgenic mouse model with early progressive vascular NOTCH3 accumulation.
Lesnik Oberstein et al., Leiden, Netherlands. In Acta Neuropathol Commun, 2014
INTRODUCTION: 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.
Exosome transfer from stromal to breast cancer cells regulates therapy resistance pathways.
Minn et al., Philadelphia, United States. In Cell, 2014
In parallel, stromal cells also activate NOTCH3 on BrCa cells.
Genetic landscape of esophageal squamous cell carcinoma.
He et al., Beijing, China. In Nat Genet, 2014
The Hippo and Notch pathways were dysregulated by mutations in FAT1, FAT2, FAT3 or FAT4 (27%) or AJUBA (JUB; 7%) and NOTCH1, NOTCH2 or NOTCH3 (22%) or FBXW7 (5%), respectively.
[Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)].
Lee et al., In Acta Neurol Taiwan, 2014
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most prevalent monogenic cerebral small vessel diseases caused by a mutation in the NOTCH3 gene.
Therapeutic modulation of Notch signalling--are we there yet?
Lendahl et al., Stockholm, Sweden. In Nat Rev Drug Discov, 2014
Deregulated Notch signalling leads to various diseases, such as T cell leukaemia, Alagille syndrome and a stroke and dementia syndrome known as CADASIL, and so strategies to therapeutically modulate Notch signalling are of interest.
Investigation of NOTCH4 coding region polymorphisms in sporadic inclusion body myositis.
Allcock et al., Perth, Australia. In J Neuroimmunol, 2012
the NOTCH4 polymorphisms, the minor allele of rs422951 and the 12-repeat variation for rs72555375, can be considered to be markers for sporadic inclusion body myositis susceptibility
Profiling immunohistochemical expression of NOTCH1-3, JAGGED1, cMET, and phospho-MAPK in 100 carcinomas of unknown primary.
Pavlidis et al., Thessaloníki, Greece. In Clin Exp Metastasis, 2012
immunohistochemical analysis of NOTCH1-3, JAGGED1, cMET, and phospho-MAPK in 100 carcinomas of unknown primary
Notch is the key factor in the process of fetal liver stem/progenitor cells differentiation into hepatocytes.
Dou et al., Xi'an, China. In Dev Growth Differ, 2012
These findings imply that Notch3 may not only be a regulator of fetal liver stem/progenitor cells differentiation into hepatocytes, but also be a potential marker of fetal liver stem/progenitor cells.
Notch2 and Notch3 function together to regulate vascular smooth muscle development.
Lilly et al., Columbus, United States. In Plos One, 2011
In vitro analysis show that both Notch2 and Notch3 robustly activate smooth muscle differentiation genes, and Notch3, but not Notch2 is a target of Notch signaling
Identification of a known mutation in Notch 3 in familiar CADASIL in China.
Liu et al., Harbin, China. In Plos One, 2011
Members of a 5-generational Han Chinese family with CADASIL patients had an R133C mutation in the NOTCH3 gene but only individuals exposed to known vascular risk factors developed CADASIL.
Notch3 signaling promotes the development of pulmonary arterial hypertension.
Thistlethwaite et al., San Diego, United States. In Nat Med, 2009
this study demonstrated that high steady-state levels of NOTCH3 are associated with the development of PAH in humans and that Notch3 expression is required for the development of pulmonary hypertension in two experimental models of this disease
Bousser et al., Paris, France. In Lancet Neurol, 2009
NOTCH3 (Notch homolog 3), the gene involved in CADASIL, encodes a transmembrane receptor primarily expressed in systemic arterial smooth-muscle cells.
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