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Mouse (Murine) NOTCH2 Protein expressed in CHO Cells - ABIN1344244
Fiorini, Merck, Wilson, Ferrero, Jiang, Koch, Auderset, Laurenti, Tacchini-Cottier, Pierres, Radtke, Luther, Macdonald: Dynamic regulation of notch 1 and notch 2 surface expression during T cell development and activation revealed by novel monoclonal antibodies. in Journal of immunology (Baltimore, Md. : 1950) 2009
These data demonstrated fascin (show FSCN1 Proteins) as a critical regulator of breast cancer stem cell pool at least partially via activation of the Notch (show NOTCH1 Proteins) self-renewal signaling pathway.
Examination of the molecular underpinnings of this "NOTCH2-BCR (show BCR Proteins) axis" in cGVHD revealed imbalanced expression of the transcription factors IRF4 (show IRF4 Proteins) and IRF8 (show IRF8 Proteins), each critical to B (show TDO2 Proteins)-cell differentiation and fate. All-trans retinoic acid (ATRA) increased IRF4 (show IRF4 Proteins) expression, restored the IRF4 (show IRF4 Proteins)-to-IRF8 (show IRF8 Proteins) ratio, abrogated BCR (show BCR Proteins)-NOTCH (show NOTCH1 Proteins) hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability.
Genetic variation in NOTCH2 was associated with troponin T levels in women with psychosis.
miR (show MLXIP Proteins)-34a expression is silenced epigenetically by EZH2 (show EZH2 Proteins) and DNA methylation (show HELLS Proteins), which promotes cholangiocarcinoma cell growth through activation of the Notch (show NOTCH1 Proteins) pathway.
Human biliary atresia and 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC (show DDC Proteins))-induced experimental cholestasis in mice are associated with increased expression of Notch2.
In conclusion, Notch (show NOTCH1 Proteins) siganling appears to be an important mediator of the liver inflammation by modulating hepatic IL-22 (show IL22 Proteins)-secreting NKp46 (show NCR1 Proteins)(+) innate lymphoid cells.
The data showed that the overexpression of miR (show MLXIP Proteins)-18a-5p could downregulate Notch2 expression and subsequently suppress endothelial-mesenchymal transition and cardiac fibrosis.
Major genomic mutation profiles in lacrimal gland adenoid cystic carcinoma (LGACC) were uncovered by exome-seq. Although preliminary in nature, the Notch (show NOTCH1 Proteins) pathway could be a potential therapeutic target for LGACC.
Data indicate that mRNA high expression level of Notch1 (show NOTCH1 Proteins) 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 Proteins)), HR, and mRNA high expression levels of Notch2 and Notch3 (show NOTCH3 Proteins) were associated with worsen OS for all NSCLC, and mRNA high expression level of Notch4 (show NOTCH4 Proteins) was not found to be associated with to OS for all NSCLC.
Mutation in NOTCH2 gene is associated with nodal marginal zone lymphoma.
Notch2 physiologically regulates bone remodeling by inhibiting trabecular bone formation in the appendicular skeleton.
Notch2 was crucial in maintaining the integrity of the epithelial and smooth muscle layers of the distal conducting airways, and our data suggest that epithelial Notch (show NOTCH1 Proteins) signaling regulates multiple aspects of postnatal development in the distal lung and may represent a potential target for intervention in pulmonary diseases.
Authors confirmed that NOTCH2 is significantly over-expressed in EEA. In the most relevant endometrial adenocarcinoma cell model, Ishikawa H, altering miR (show MLXIP Proteins)-181c expression produces significant changes in NOTCH2 expression, consistent with direct targeting.
These findings highlight the molecular basis of Hajdu-Cheney syndrome (HCS (show HLCS Proteins)) pathogenesis and provide clinical insights into potential targeted therapeutic strategies for skeletal disorders associated with the aberrant FBW7 (show FBXW7 Proteins)/NOTCH2 pathway as observed in patients with HCS (show HLCS Proteins).
Hajdu-Cheney Syndrome is a devastating disease associated with a gain-of-NOTCH2 function resulting in diverse clinical manifestations
Lnc-LFAR1 binds directly to Smad2 (show SMAD2 Proteins)/3 and promotes transcription of TGFbeta (show TGFB1 Proteins), Smad2 (show SMAD2 Proteins), Smad3 (show SMAD3 Proteins), Notch2 and Notch3 (show NOTCH3 Proteins) which, in turn, results in TGFbeta (show TGFB1 Proteins) and Notch (show NOTCH1 Proteins) pathway activation.
Study indicates that knockdown of Notch2 promotes in vivo growth of triple-negative breast cancer (TNBC) and proposes that Notch2 functions as a tumor growth suppressor in TNBC.
this study shows that Notch (show NOTCH1 Proteins) signaling regulates basophils biological function, at least partially via the modulation of MAPK (show MAPK1 Proteins)
Postnatal development analysis revealed that in cilia-deficient corneal epithelial cells downregulation of the Notch (show NOTCH1 Proteins) pathway precedes cell proliferation defects.
bovine herpesvirus 1 ORF2 protein reduced the trans-activation potential of Notch1 (show NOTCH1 Proteins) and Notch3 (show NOTCH3 Proteins), suggesting that ORF2 interfered with the trans-activation potential of Notch (show NOTCH1 Proteins).
DeltaC/Notch1a and Notch2 signaling is responsible for a survival signal provided by xanthophores to melanophores.
This gene encodes a member of the Notch family. Members of this Type 1 transmembrane protein family share structural characteristics including an extracellular domain consisting of multiple epidermal growth factor-like (EGF) repeats, and an intracellular domain consisting of multiple, different domain types. Notch family members play a role in a variety of developmental processes by controlling cell fate decisions. The Notch signaling network is an evolutionarily conserved intercellular signaling pathway which regulates interactions between physically adjacent cells. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signaling pathway that plays a key role in development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remain to be determined. This protein is cleaved in the trans-Golgi network, and presented on the cell surface as a heterodimer. This protein functions as a receptor for membrane bound ligands, and may play a role in vascular, renal and hepatic development. Two transcript variants encoding different isoforms have been found for this gene.
, neurogenic locus notch homolog protein 2-like
, Notch homolog 2
, neurogenic locus notch homolog protein 2
, Motch B
, Notch gene homolog 2
, notch gene homolog 2
, notch receptor protein 6