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anti-Human NOTCH3 Antibodies:
anti-Mouse (Murine) NOTCH3 Antibodies:
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Human Monoclonal NOTCH3 Primary Antibody for ELISA, WB - ABIN562028
Park, Shih, Wang: Identification of Pbx1, a potential oncogene, as a Notch3 target gene in ovarian cancer. in Cancer research 2008
Show all 7 Pubmed References
Human Polyclonal NOTCH3 Primary Antibody for IHC - ABIN966685
Joutel, Corpechot, Ducros, Vahedi, Chabriat, Mouton, Alamowitch, Domenga, Cécillion, Marechal, Maciazek, Vayssiere, Cruaud, Cabanis, Ruchoux, Weissenbach, Bach, Bousser, Tournier-Lasserve: Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia. in Nature 1996
Show all 3 Pubmed References
Human Polyclonal NOTCH3 Primary Antibody for IHC - ABIN966682
Gray, Mann, Mitsiadis, Henrique, Carcangiu, Banks, Leiman, Ward, Ish-Horowitz, Artavanis-Tsakonas: Human ligands of the Notch receptor. in The American journal of pathology 1999
Show all 3 Pubmed References
Mouse (Murine) Monoclonal NOTCH3 Primary Antibody for FACS - ABIN2475922
Droese, Pape, Stolley: [Lipic content and fatty acid pattern in human milk and cow's milk (author's transl)]. in European journal of pediatrics 1976
Show all 4 Pubmed References
Human Polyclonal NOTCH3 Primary Antibody for IHC (fro), IHC - ABIN408754
Soylu, Acar, Ozbey, Unal, Koksal, Bassorgun, Ciftcioglu, Ustunel: Characterization of Notch Signalling Pathway Members in Normal Prostate, Prostatic Intraepithelial Neoplasia (PIN) and Prostatic Adenocarcinoma. in Pathology oncology research : POR 2015
Human Polyclonal NOTCH3 Primary Antibody for IHC (p), IP - ABIN250809
Dang, Fan, Chaudhry, Wang, Gaiano, Eberhart: Notch3 signaling initiates choroid plexus tumor formation. in Oncogene 2006
Human Monoclonal NOTCH3 Primary Antibody for CyTOF, FACS - ABIN4900322
Soriani, Iannitto, Ricci, Fionda, Malgarini, Morrone, Peruzzi, Ricciardi, Petrucci, Cippitelli, Santoni: Reactive oxygen species- and DNA damage response-dependent NK cell activating ligand upregulation occurs at transcriptional levels and requires the transcriptional factor E2F1. in Journal of immunology (Baltimore, Md. : 1950) 2014
Oligodendrocytes expressing mutant NOTCH3(R90C) (present in CADASIL disease), exhibited aberrant NOTCH3 proteolytic processing. These cells were less viable and had a higher rate of apoptosis. Cells with NOTCH3(R90C) had higher levels of intrinsic mitochondrial apoptosis, extrinsic death receptor path-related apoptosis, and autophagy compared with cells transfected with wild-type NOTCH3.
Novel variants in NOTCH3 associated with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
NOTCH3 single-nucleotide polymorphisms role in susceptibility to non-small cell lung cancer
Single-nucleotide polymorphism in NOTCH3 gene is associated with breast cancers.
Reduced NOTCH3/NICD3 and NOTCH4 (show NOTCH4 Antibodies)/NICD4 in miR (show MLXIP Antibodies)-96- and miR (show MLXIP Antibodies)-183-expressing nasopharyngeal carcinoma (NPC (show NPC1 Antibodies)) cells suggest the involvement of the NOTCH (show NOTCH1 Antibodies) signaling pathway in their tumor suppressive function.
ChIP-seq studies show a high concordance of functional NOTCH1 (show NOTCH1 Antibodies) and NOTCH3 genomic binding sites that are enriched in binding motifs for RBPJ (show RBPJ Antibodies), the transcription factor that recruits activated Notch (show NOTCH1 Antibodies) to DNA. The interchangeability of NOTCH1 (show NOTCH1 Antibodies) and NOTCH3 was confirmed by rescue of NOTCH1 (show NOTCH1 Antibodies)-dependent T-ALL cells with activated NOTCH3 and vice versa.
Low Notch3 expression is associated with left ventricle hypertrabeculation/non-compaction and Menetrier-like gastropathy.
High NOTCH3 expression is associated with basal breast cancer.
in in silico gene expression analysis of human T-ALL samples we observed a significant correlation between Pin1 (show PIN1 Antibodies) and Notch3 expression levels, which may further suggest a key role of the newly identified Notch3-Pin1 (show PIN1 Antibodies) axis in T-cell Acute Lymphoblastic Leukemia (T-ALL) aggressiveness and progression. Thus, combined suppression of Pin1 (show PIN1 Antibodies) and Notch3 proteins may be exploited as an additional target therapy for T-ALL
Data indicate that mRNA high expression level of Notch1 (show NOTCH1 Antibodies) was associated with better overall survival (OS) for all NSCLC, hazard ratio (HR), better OS in adenocarcinoma (Ade), HR, as well as in squamous cell carcinoma (SCC (show CYP11A1 Antibodies)), HR, and mRNA high expression levels of Notch2 (show NOTCH2 Antibodies) and Notch3 were associated with worsen OS for all NSCLC, and mRNA high expression level of Notch4 (show NOTCH4 Antibodies) was not found to be associated with to OS for all NSCLC.
Notch3 mutation impairs recovery of cardiac function post-myocardial ischemia.
Notch3 plays an important role in the maintenance of quiescent neural stem cells in the subependymal zone.
Lnc-LFAR1 binds directly to Smad2 (show SMAD2 Antibodies)/3 and promotes transcription of TGFbeta (show TGFB1 Antibodies), Smad2 (show SMAD2 Antibodies), Smad3 (show SMAD3 Antibodies), Notch2 (show NOTCH2 Antibodies) and Notch3 which, in turn, results in TGFbeta (show TGFB1 Antibodies) and Notch (show NOTCH1 Antibodies) pathway activation.
this study shows that Notch (show NOTCH1 Antibodies) signaling regulates basophils biological function, at least partially via the modulation of MAPK (show MAPK1 Antibodies)
Knock-in mice with the R169C mutation (Notch3(R170C/R170C)) exhibited similar reductions in arterial lumen, and both TgNotch3(R169C) and Notch3(R170C/R170C) mice showed increased cerebral artery expression of Notch3 target genes.
Notch3 is an important protective factor for cardiac fibrosis in a myocardial infarction model, and the protective effect of Notch3 is attributable to its action on TGF-beta1 (show TGFB1 Antibodies)/Smad3 (show SMAD3 Antibodies) signaling.
Data indicate that Notch (show NOTCH1 Antibodies) receptors Notch1 (show NOTCH1 Antibodies) and Notch3 deficiency compromises pericyte function and contributes to vascular pathologies.
In this study, authors use a smooth muscle-specific (show EIF3K Antibodies) deletion of Notch2 (show NOTCH2 Antibodies) together with a global Notch3 deletion to produce mice with combinations of mutant and wild-type Notch2 (show NOTCH2 Antibodies)/3 alleles in vascular smooth muscle cells
Elevated levels of TIMP3 (show TIMP3 Antibodies) and vitronectin (show VTN Antibodies), acting downstream of Notch3(ECD (show ECD Antibodies)) deposition, play a role in CADASIL, producing divergent influences on early CBF (show CEBPZ Antibodies) deficits and later white matter lesions.
Mutant Notch3 accumulates in pericytes and causes progressive pericyte loss and BBB (show ALMS1 Antibodies) leakage in the cerebral cortex in CADASIL mouse model.
The Notch3 receptor is required earlier within the developing somite to regulate hematopoietic stem cell (HSC (show FUT1 Antibodies)) emergence in a non-cell-autonomous manner.
90 % of proliferating radial glia express notch1a (show NOTCH1A Antibodies), notch1b and notch3. In contrast, the proliferating non-glial populations of the dorsal telencephalon and hypothalamus rarely express notch3 and about half express notch1a (show NOTCH1A Antibodies)/1b.
Notch3 regulates oligodendrocyte precursor cells development and mbp (show MBP Antibodies) gene expression in larvae, and maintains vascular integrity in adults.
new role for Notch (show NOTCH1 Antibodies) signaling in brain vascular development whereby Notch3 signaling promotes expansion of the brain pericyte population
Notch3 activity gates neural stem cell activation in the adult pallium.
Cellular correlates of Notch (show NOTCH1 Antibodies)-delta gene expression in the regenerating zebrafish retina.
knockdown of notch3 function in notch1a (show NOTCH1A Antibodies) mutants leads to the loss of rhombomere boundary cells and causes neuronal hyperplasia
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).
Notch homolog 3
, neurogenic locus notch homolog protein 3
, Notch gene homolog 3