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Examination of the molecular underpinnings of this "NOTCH2-BCR (show BCR ELISA Kits) axis" in cGVHD revealed imbalanced expression of the transcription factors IRF4 (show IRF4 ELISA Kits) and IRF8 (show IRF8 ELISA Kits), each critical to B (show TDO2 ELISA Kits)-cell differentiation and fate. All-trans retinoic acid (ATRA) increased IRF4 (show IRF4 ELISA Kits) expression, restored the IRF4 (show IRF4 ELISA Kits)-to-IRF8 (show IRF8 ELISA Kits) ratio, abrogated BCR (show BCR ELISA Kits)-NOTCH (show NOTCH1 ELISA Kits) 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 ELISA Kits)-34a expression is silenced epigenetically by EZH2 (show EZH2 ELISA Kits) and DNA methylation (show HELLS ELISA Kits), which promotes cholangiocarcinoma cell growth through activation of the Notch (show NOTCH1 ELISA Kits) pathway.
Human biliary atresia and 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC (show DDC ELISA Kits))-induced experimental cholestasis in mice are associated with increased expression of Notch2.
In conclusion, Notch (show NOTCH1 ELISA Kits) siganling appears to be an important mediator of the liver inflammation by modulating hepatic IL-22 (show IL22 ELISA Kits)-secreting NKp46 (show NCR1 ELISA Kits)(+) innate lymphoid cells.
The data showed that the overexpression of miR (show MLXIP ELISA Kits)-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 ELISA Kits) pathway could be a potential therapeutic target for LGACC.
Data indicate that mRNA high expression level of Notch1 (show NOTCH1 ELISA Kits) 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 ELISA Kits)), HR, and mRNA high expression levels of Notch2 and Notch3 (show NOTCH3 ELISA Kits) were associated with worsen OS for all NSCLC, and mRNA high expression level of Notch4 (show NOTCH4 ELISA Kits) was not found to be associated with to OS for all NSCLC.
Mutation in NOTCH2 gene is associated with nodal marginal zone lymphoma.
Transgenic mice harboring Notch2 mutation analogous to that in patients with Hajdu-Cheney syndrome (HCS (show HLCS ELISA Kits)) are severely osteopenic because of enhanced bone resorption; this model has now been validated. Data from further studies in transgenic mice suggest that the HCS (show HLCS ELISA Kits) mutation in osteoblasts, but not in osteoclasts, causes osteopenia in this model.
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 ELISA Kits)/3 and promotes transcription of TGFbeta (show TGFB1 ELISA Kits), Smad2 (show SMAD2 ELISA Kits), Smad3 (show SMAD3 ELISA Kits), Notch2 and Notch3 (show NOTCH3 ELISA Kits) which, in turn, results in TGFbeta (show TGFB1 ELISA Kits) and Notch (show NOTCH1 ELISA Kits) 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 ELISA Kits) signaling regulates basophils biological function, at least partially via the modulation of MAPK (show MAPK1 ELISA Kits)
Postnatal development analysis revealed that in cilia-deficient corneal epithelial cells downregulation of the Notch (show NOTCH1 ELISA Kits) pathway precedes cell proliferation defects.
these results show that ADAM10 (show ADAM10 ELISA Kits)-Notch (show NOTCH1 ELISA Kits) signaling in ovarian somatic cells governs the primordial follicle formation by controlling the development of ovarian pregranulosa cells.
Notch1 (show NOTCH1 ELISA Kits) and Notch2 are the primary Notch (show NOTCH1 ELISA Kits) receptors regulating epithelial cell homoeostasis in mouse and human stomach.
bovine herpesvirus 1 ORF2 protein reduced the trans-activation potential of Notch1 (show NOTCH1 ELISA Kits) and Notch3 (show NOTCH3 ELISA Kits), suggesting that ORF2 interfered with the trans-activation potential of Notch (show NOTCH1 ELISA Kits).
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