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anti-Human RBPJ Anticorps:
anti-Mouse (Murine) RBPJ Anticorps:
anti-Rat (Rattus) RBPJ Anticorps:
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Human Monoclonal RBPJ Primary Antibody pour WB - ABIN2668739
Maier, Santak, Mantik, Grabusic, Kremmer, Hammerschmidt, Kempkes et al.: A somatic knockout of CBF1 in a human B-cell line reveals that induction of CD21 and CCR7 by EBNA-2 is strictly CBF1 dependent and that downregulation of immunoglobulin M is partially CBF1 ... dans Journal of virology 2005
Human Monoclonal RBPJ Primary Antibody pour ChIP, EMSA - ABIN2668822
Ehm, Göritz, Covic, Schäffner, Schwarz, Karaca, Kempkes, Kremmer, Pfrieger, Espinosa, Bigas, Giachino, Taylor, Frisén, Lie: RBPJkappa-dependent signaling is essential for long-term maintenance of neural stem cells in the adult hippocampus. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 2010
Variants rs2270226 and rs2077777 in the RBPJ gene were associated with the risk of cerebral infarction diseases in the Chinese Han population.
RBPJ and MAML3 (Montrer MAML3 Anticorps) could be new therapeutic targets for SCLC.
The ULK3 (Montrer ULK3 Anticorps) Kinase Is Critical for Convergent Control of Cancer-Associated Fibroblast Activation by CSL (Montrer CSHL1 Anticorps) and GLI (Montrer GLI1 Anticorps)
Notch1 signaling plays an important role in the maintenance of the cancer stem-like phenotype in diffuse type gastric cancer through an RBP-Jkappa dependent pathway; inhibiting Notch1 signaling could be an effective therapy against CD133 positive diffuse type gastric cancers
We show that GIT1, which also contains an ANK (Montrer ANK1 Anticorps) domain, inhibits the Notch1 (Montrer NOTCH1 Anticorps)-Dll4 (Montrer DLL4 Anticorps) signaling pathway by competing with Notch1 (Montrer NOTCH1 Anticorps) ANK (Montrer ANK1 Anticorps) domain for binding to RBP-J in stalk cells
we report that genetic removal of CSL (Montrer CSHL1 Anticorps) in breast tumor cells caused accelerated growth of xenografted tumors. Loss of CSL (Montrer CSHL1 Anticorps) unleashed a hypoxic response during normoxic conditions, manifested by stabilization of the HIF1alpha (Montrer HIF1A Anticorps) protein and acquisition of a polyploid giant-cell, cancer stem cell-like, phenotype.
RBPJ interacts with L3MBTL3 (Montrer L3MBTL3 Anticorps) to promote repression of Notch (Montrer NOTCH1 Anticorps) signaling via histone demethylase (Montrer MBD2 Anticorps) KDM1A (Montrer KDM1A Anticorps).
RBPJ links MYC (Montrer MYC Anticorps) and transcriptional control through CDK9 (Montrer CDK9 Anticorps) in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH (Montrer NOTCH1 Anticorps)
Mean CBF1 expression is significantly increased in isocitrate dehydrogenase 1 (IDH1 (Montrer IDH1 Anticorps)) R132H mutant glioblastoma. Hypoxic regions of glioblastoma have higher CBF1 activation and exposure to low oxygen can induce its expression in glioma cells in vitro.
structural and biophysical studies demonstrate that RITA (Montrer ZNF331 Anticorps) binds RBP-J similarly to the RAM (Montrer RAB27A Anticorps) (RBP-J-associated molecule) domain of Notch (Montrer NOTCH1 Anticorps), our biochemical and cellular assays suggest that RITA (Montrer ZNF331 Anticorps) interacts with additional regions in RBP-J.
Early pancreatic islet fate and maturation is controlled through RBP (Montrer RBP4 Anticorps)-Jkappa.
In this study, the authors found that conditional disruption of RBP-J, the transcription factor of canonical Notch (Montrer NOTCH1 Anticorps) signaling, increased irradiation sensitivity in mice.
Data (including data from studies in transgenic mice) suggest that signaling via Notch2 (Montrer NOTCH2 Anticorps) and Notch3 (Montrer NOTCH3 Anticorps) plays role in promoting cell differentiation and steroidogenesis in preovulatory granulosa cells; mechanism involves regulation of gene expression of Jag1 (Montrer JAG1 Anticorps) and Rbpj. (Notch2 (Montrer NOTCH2 Anticorps) = Notch2 (Montrer NOTCH2 Anticorps) receptor; Notch3 (Montrer NOTCH3 Anticorps) = Notch3 (Montrer NOTCH3 Anticorps) receptor; Jag1 (Montrer JAG1 Anticorps) = jagged-1 (Montrer JAG1 Anticorps) protein; Rbpj = recombining binding protein suppressor of hairless)
Macrophage maturation is controlled by Notch ligand (Montrer JAG2 Anticorps) Dll1 (Montrer DLL1 Anticorps) expressed in vascular endothelial cells of arteries and requires macrophage canonical Notch (Montrer NOTCH1 Anticorps) signaling via Rbpj, which simultaneously suppresses an inflammatory macrophage fate. Conversely, conditional mutant mice lacking Dll1 (Montrer DLL1 Anticorps) or Rbpj show proliferation and transient accumulation of inflammatory macrophages, which antagonizes arteriogenesis and tissue repair.
RBPJ binds and trans-activates the Il23r (Montrer IL23R Anticorps) promoter and induces IL-23R (Montrer IL23R Anticorps) expression and represses anti-inflammatory IL-10 (Montrer IL10 Anticorps) production in Th17 cells.
RBP-J deficiency drastically reduced dopamine release in the striatum and caused a subtle decrease in the number of dopaminergic neurons. These findings demonstrated that Notch (Montrer NOTCH1 Anticorps)/RBP-J signaling regulates dopamine responsiveness in the striatum, which may explain the mechanism whereby Notch (Montrer NOTCH1 Anticorps)/RBP-J signaling affects an individual's susceptibility to neuropsychiatric disease.
RBP-J-mediated Notch (Montrer NOTCH1 Anticorps) signalling is critical for basophil-dependent immunoregulation. Deficiency of RBP-J influences the immunoregulatory functions of BA, which include activation of T cells and their differentiation into T helper cell subtypes.
Data, including data from studies using cells from transgenic/knockout mice, suggest that Med1 (Montrer MBD4 Anticorps) plays role in enamel formation; Med1 (Montrer MBD4 Anticorps) induces Alpl (Montrer ALPL Anticorps) via stimulation of Notch1 (Montrer NOTCH1 Anticorps) signaling by forming Notch1 (Montrer NOTCH1 Anticorps)-RBP-Jk complex on Alpl (Montrer ALPL Anticorps) promoter. (Med1 (Montrer MBD4 Anticorps) = mediator complex subunit 1 (Montrer MED1 Anticorps); Alpl (Montrer ALPL Anticorps) = alkaline phosphatase, liver-bone-kidney; Notch1 (Montrer NOTCH1 Anticorps) = Notch gene homolog 1 (Montrer NOTCH1 Anticorps); RBP-Jk = kappa J region recombining binding protein suppressor of hairless)
study uncovered a regulatory network, where miR (Montrer MLXIP Anticorps)-182 functions as an important new node that receives inputs from RBP-J and TNF-alpha (Montrer TNF Anticorps) signaling and positively regulates inflammatory osteoclastogenesis; suppression of miR (Montrer MLXIP Anticorps)-182 by RBP-J serves as an important mechanism that restrains TNF-alpha (Montrer TNF Anticorps) induced osteoclastogenesis
structural and biophysical studies demonstrate that RITA (Montrer C12orf52 Anticorps) binds RBP-J similarly to the RAM (Montrer FAM103A1 Anticorps) (RBP-J-associated molecule) domain of Notch (Montrer NOTCH1 Anticorps), our biochemical and cellular assays suggest that RITA (Montrer C12orf52 Anticorps) interacts with additional regions in RBP-J.
findings reveal that, in response to Wnt (Montrer WNT2 Anticorps) signalling, Dishevelled (Montrer DVL2 Anticorps) inhibits CSL (Montrer SMPX Anticorps) transcription factors to regulate Notch (Montrer NOTCH1 Anticorps) signalling and cell-fate decisions in vivo
The study reports the identification and functional characterization of rbpj interacting and tubulin associated (RITA) (C12ORF52 (Montrer C12orf52 Anticorps)) as a novel rbpj/CBF-1-interacting protein.
The results suggest that a cell-to-cell interaction via the Notch (Montrer NOTCH1 Anticorps)/Su(H) pathway has a significant role in the PGC (Montrer PGC Anticorps) migration by regulating cell motility.
This "target protector and rescue assay" demonstrates that the phenotypic defects associated with CUGBP1 inactivation in Xenopus are essentially due to the deregulation of Su(H) mRNA.
Intronic Flk1 (Montrer KDR Anticorps) genetic enhancer element directs arterial-specific expression via RBPJ-mediated venous repression.
embryos treated with morpholinos against wt1a, foxc1a, or the Notch (Montrer NOTCH1 Anticorps) transcriptional mediator rbpj develop fewer podocytes, as determined by wt1b (Montrer WT1 Anticorps), hey1 (Montrer HEY1 Anticorps) and nephrin (Montrer NPHS1 Anticorps) expression, while embryos deficient in any two of these factors completely lack podocytes
her8a is positively regulated by Su(H)-dependent Notch (Montrer NOTCH1 Anticorps) signaling as revealed by a Notch (Montrer NOTCH1 Anticorps)-defective mutant and injection of variants of the Notch (Montrer NOTCH1 Anticorps) intracellular regulator, Su(H).
analysed the function of Su(H) in the somitogenesis process and its influence on the expression of notch (Montrer NOTCH1 Anticorps) pathway genes
one element of the Notch (Montrer NOTCH1 Anticorps) signalling pathway, Su(H), is required for control of retinoic acid metabolism in the tailbud
The protein encoded by this gene is a transcriptional regulator important in the Notch signaling pathway. The encoded protein acts as a repressor when not bound to Notch proteins and an activator when bound to Notch proteins. It is thought to function by recruiting chromatin remodeling complexes containing histone deacetylase or histone acetylase proteins to Notch signaling pathway genes. Also, this protein can bind specifically to the recombination signal sequence of immunglobulin kappa type J segments. Several transcript variants encoding different isoforms have been found for this gene, and several pseudogenes of this gene exist on chromosome 9.
, H-2K binding factor-2
, RBP-J kappa
, immunoglobulin kappa J region recombination signal binding protein 1
, recombining binding protein suppressor of hairless
, renal carcinoma antigen NY-REN-30
, suppressor of hairless homolog
, J kappa-recombination signal-binding protein
, suppressor of hairless protein 1
, suppressor of hairless protein homolog
, recombination signal binding protein for immunoglobulin kappa J region a
, suppressor of hairless 2
, recombining binding protein suppressor of hairless-like