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anti-Human NOTCH2 Antibodies:
anti-Mouse (Murine) NOTCH2 Antibodies:
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Human Polyclonal NOTCH2 Primary Antibody for IHC (p), IHC - ABIN5695614
Chen, Oh, Hinman, Abraham: Visualization of APP dimerization and APP-Notch2 heterodimerization in living cells using bimolecular fluorescence complementation. in Journal of neurochemistry 2006
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Human Polyclonal NOTCH2 Primary Antibody for EIA, IHC (p) - ABIN615149
Schwamborn, Müller, Becker, Püschel: Ubiquitination of the GTPase Rap1B by the ubiquitin ligase Smurf2 is required for the establishment of neuronal polarity. in The EMBO journal 2007
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Human Polyclonal NOTCH2 Primary Antibody for IHC, ELISA - ABIN104900
Gupta, Li, Abedin, Wang, Schneider, Najafian, Rosenberg: Effect of Notch activation on the regenerative response to acute renal failure. in American journal of physiology. Renal physiology 2009
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Human Polyclonal NOTCH2 Primary Antibody for EIA, IF - ABIN303122
Siar, Ha, Aung, Nakano, Tsujigiwa, Nagatsuka, Ng, Kawakami: Immunolocalization of notch signaling protein molecules in a maxillary chondrosarcoma and its recurrent tumor. in European journal of medical research 2010
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Mouse (Murine) Monoclonal NOTCH2 Primary Antibody for FACS - ABIN2475916
Bataille, Rosselin, Freychet: Interactions of glucagon, gut glucagon, vasoactive intestinal polypeptide and secretin with their membrane receptors. in Israel journal of medical sciences 1975
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Human Monoclonal NOTCH2 Primary Antibody for FACS - ABIN1169006
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
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Human Polyclonal NOTCH2 Primary Antibody for ELISA, WB - ABIN104899
Bertrand, Eckfeldt, Lysholm, LeBien: Notch-1 and Notch-2 exhibit unique patterns of expression in human B-lineage cells. in Leukemia 2001
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Cow (Bovine) Polyclonal NOTCH2 Primary Antibody for WB - ABIN2777549
Tilley, Harvey, Heguy, Hackett, Wang, OConnor, Crystal: Down-regulation of the notch pathway in human airway epithelium in association with smoking and chronic obstructive pulmonary disease. in American journal of respiratory and critical care medicine 2009
Dog (Canine) Polyclonal NOTCH2 Primary Antibody for ELISA - ABIN547569
Schwarzmeier, Hubmann, Düchler, Jäger, Shehata: Regulation of CD23 expression by Notch2 in B-cell chronic lymphocytic leukemia. in Leukemia & lymphoma 2004
Reduced monocyte NOTCH2 expression in neutralizing antidrug antibodies (nADA)+ multiple sclerosis patients was associated with NOTCH2. NOTCH2 activation was T cell dependent and was only triggered in the presence of serum from nADA+ patients. Thus, nADA development was driven by a proinflammatory environment that triggered activation of the NOTCH2 signaling pathway prior to first IFN-beta administration.
Notch2 depletion significantly reduced the mesenchymal stem cell-mediated radio-protective effect in human- and mouse-derived hematopoietic progenitor/stem cell.
Notch2 expression is associated with neural stem cells differentiation status.
Further studies verified that miR-1 regulates EMT signalling pathways directly through Notch2. Therefore, these results confirm that, as a tumor suppressor gene, miR-1 may be a potential tumor marker for the early diagnosis of esophageal squamous cell carcinoma and a new drug target
MINAR1 physically interacts with Notch2 and its binding to Notch2 increases its stability and function.
Review of the roles of NOTCH1 and NOTCH2 in urinary bladder cancer suggests that NOTCH1 acts as a tumor suppressor and NOTCH2 acts as an oncogene that promotes cell proliferation and metastasis through epithelial-to-mesenchymal transition, cell cycle progression, and maintenance of stemness.
Increase in Notch2 expression in RANKL-predominant periapical lesions corroborates their joined involvement in extensive periapical bone resorption.
Jag1 and Notch2 play a key role in kidney fibrosis development by regulating Tfam expression and metabolic reprogramming.
ectopic miR-181b expression suppressed cancer stem cell properties and enhanced sensitivity to cisplatin (DDP) treatment by directly targeting Notch2. miR-181b could inactivate the Notch2/Hes1 signalling pathway.
that miR-1-5p acted as a suppressive miRNA and played vital roles in the growth, migration and invasion of gallbladder carcinoma cell through targeting Notch2
Notch2 activation in the microenvironment is a pre-requisite for the activation of canonical Wnt signalling in tumour cells.
TNFalpha regulates NOTCH2 and NOTCH3 expression in pulmonary artery smooth muscle cells via preferential ACTR-IIA signalling in BMPR-II-deficient cells.
results confirm the association of the NOTCH2-mutation with shorter median treatment-free survival and suggest the possible usefulness of the identification of these changes for the diagnosis of splenic marginal zone lymphoma.
In conclusion, we demonstrated that EV71 infection induced elevated expressions of TLR3/4 and Notch1/2 in CD14+ monocytes.
ATRX, NOTCH1 and NOTCH2 expression varies in angiosarcomas and shows significant correlations with site of origin and poor clinical outcome
BANCR may promote melanoma cell growth through inhibition of miR204, leading to the activation of Notch2 pathway. Authors further demonstrated that BANCR knockdown inhibited tumor growth in vivo. Results suggest the BANCR/miR204/Notch2 axis mediates melanoma cell proliferation and tumor progression.
Altered expression of WFS1 and NOTCH2 genes may play a role in pathogenesis and development of DN in patients with T2DM.
IRF4 is overexpressed in human non-small cell lung cancer and activates the Notch signaling pathway.
Notch2 is important in Club cell differentiation in normal lungs and adenocarcinoma. Notch2 is regulated mutually with Notch1, and the balance of the expression of Notch receptors could determine the biological behaviours of lung cancer cells.
Notch2 is up-regulated in oesophageal squamous cell carcinoma tissues and could serve as a promising biomarker for identifying individuals with poor prognostic potential.
mutational activation of Notch2 does not directly control osteoblast activity but favors a pro-osteoclastic gene expression pattern, which in turn triggers high bone turnover.
deletion of Notch2 in the limb mesenchyme increases both glycolysis and bone formation in the long bones of postnatal mice, whereas pharmacological reduction of glycolysis abrogates excessive bone formation.
Aberrant Notch2 expression enhances fibroblast growth factor receptor-1 (FGFR1) activity to specifically target the AKT-GSK3 signalling pathway to block apoptosis. These results have implications for understanding molecular changes involved in both tumorigenesis and therapy resistance
Identify unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways.
Notch2 is the major determinant of hepatocyte-derived intrahepatic cholangiocarcinoma formation.
Collectively, these data show that DLL4 preferentially activates NOTCH1 over NOTCH2, whereas DLL1 is equally effective in activating NOTCH1 and NOTCH2, establishing that the ectodomains dictate selective ligand function in vivo, and that features outside the known binding interface contribute to their differences.
Our findings reveal deep conservation of Jagged1-Notch2 signaling in patterning the pharyngeal arches from fish to mouse to man, despite the very different functions of their skeletal derivatives in jaw support and sound transduction.
that regulating Notch2 protein levels is particularly important during normal signaling during mouse lens development
The results suggest that CD19 controls the differentiation of marginal zone precursors to marginal zone B cells by regulating ADAM28-mediated Notch2 cleavage.
Data (including data from studies in transgenic mice) suggest that signaling via Notch2 and Notch3 plays role in promoting cell differentiation and steroidogenesis in preovulatory granulosa cells; mechanism involves regulation of gene expression of Jag1 and Rbpj. (Notch2 = Notch2 receptor; Notch3 = Notch3 receptor; Jag1 = jagged-1 protein; Rbpj = recombining binding protein suppressor of hairless)
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 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-181c expression produces significant changes in NOTCH2 expression, consistent with direct targeting.
These findings highlight the molecular basis of Hajdu-Cheney syndrome (HCS) pathogenesis and provide clinical insights into potential targeted therapeutic strategies for skeletal disorders associated with the aberrant FBW7/NOTCH2 pathway as observed in patients with HCS.
Hajdu-Cheney Syndrome is a devastating disease associated with a gain-of-NOTCH2 function resulting in diverse clinical manifestations
Lnc-LFAR1 binds directly to Smad2/3 and promotes transcription of TGFbeta, Smad2, Smad3, Notch2 and Notch3 which, in turn, results in TGFbeta and Notch 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.
bovine herpesvirus 1 ORF2 protein reduced the trans-activation potential of Notch1 and Notch3, suggesting that ORF2 interfered with the trans-activation potential of Notch.
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