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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. dans Journal of immunology (Baltimore, Md. : 1950) 2009
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.
analysis of highly recurrent genetic lesions in components of the NF-kappaB pathway, of NOTCH1 and NOTCH2 as well as KMT2D that may have a role in ocular adnexal MALT-type marginal zone lymphomas
The SNHG12/miR-195-5p/Notch2-Notch signaling pathway axis might become a novel therapeutic target for osteosarcoma. SNHG12 functioned as a competing endogenous RNA, modulating the expression of Notch2 by sponging miR-195-5p in osteosarcoma.
NOTCH2 acts as an oncogene that promotes bladder cancer growth and metastasis through epithelial-to-mesenchymal transition, cell-cycle progression, and maintenance of stemness. Inhibition of NOTCH2 is a rational novel treatment strategy for invasive bladder cancer.
These data demonstrated fascin as a critical regulator of breast cancer stem cell pool at least partially via activation of the Notch self-renewal signaling pathway.
Examination of the molecular underpinnings of this "NOTCH2-BCR axis" in cGVHD revealed imbalanced expression of the transcription factors IRF4 and IRF8, each critical to B-cell differentiation and fate. All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH 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-34a expression is silenced epigenetically by EZH2 and DNA methylation, which promotes cholangiocarcinoma cell growth through activation of the Notch pathway.
Human biliary atresia and 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-induced experimental cholestasis in mice are associated with increased expression of Notch2.
In conclusion, Notch siganling appears to be an important mediator of the liver inflammation by modulating hepatic IL-22-secreting NKp46(+) innate lymphoid cells.
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.
this study shows that Notch signaling regulates basophils biological function, at least partially via the modulation of MAPK
Postnatal development analysis revealed that in cilia-deficient corneal epithelial cells downregulation of the Notch pathway precedes cell proliferation defects.
The data showed that the overexpression of miR-18a-5p could downregulate Notch2 expression and subsequently suppress endothelial-mesenchymal transition and cardiac fibrosis.
these results show that ADAM10-Notch signaling in ovarian somatic cells governs the primordial follicle formation by controlling the development of ovarian pregranulosa cells.
Transgenic mice harboring Notch2 mutation analogous to that in patients with Hajdu-Cheney syndrome (HCS) 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 mutation in osteoblasts, but not in osteoclasts, causes osteopenia in this model.
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