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anti-Rat (Rattus) RBPJ Antibodies:
anti-Human RBPJ Antibodies:
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Human Monoclonal RBPJ Primary Antibody for 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 ... in Journal of virology 2005
Human Monoclonal RBPJ Primary Antibody for 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. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2010
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 (show ANK1 Antibodies) domain, inhibits the Notch1 (show NOTCH1 Antibodies)-Dll4 (show DLL4 Antibodies) signaling pathway by competing with Notch1 (show NOTCH1 Antibodies) ANK (show ANK1 Antibodies) domain for binding to RBP-J in stalk cells
we report that genetic removal of CSL (show CSHL1 Antibodies) in breast tumor cells caused accelerated growth of xenografted tumors. Loss of CSL (show CSHL1 Antibodies) unleashed a hypoxic response during normoxic conditions, manifested by stabilization of the HIF1alpha (show HIF1A Antibodies) protein and acquisition of a polyploid giant-cell, cancer stem cell-like, phenotype.
RBPJ interacts with L3MBTL3 (show L3MBTL3 Antibodies) to promote repression of Notch (show NOTCH1 Antibodies) signaling via histone demethylase (show MBD2 Antibodies) KDM1A (show KDM1A Antibodies).
RBPJ links MYC (show MYC Antibodies) and transcriptional control through CDK9 (show CDK9 Antibodies) in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH (show NOTCH1 Antibodies)
Mean CBF1 expression is significantly increased in isocitrate dehydrogenase 1 (IDH1 (show IDH1 Antibodies)) 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 (show ZNF331 Antibodies) binds RBP-J similarly to the RAM (show RAB27A Antibodies) (RBP-J-associated molecule) domain of Notch (show NOTCH1 Antibodies), our biochemical and cellular assays suggest that RITA (show ZNF331 Antibodies) interacts with additional regions in RBP-J.
The present findings indicate that p53 (show TP53 Antibodies), in turn, decreases CSL (show CSHL1 Antibodies) expression, which can serve to enhance p53 (show TP53 Antibodies) activity in acute DNA damage response of cells.
RBP-J mediated by miR (show MLXIP Antibodies)-133a probably contributed to the regulation of DCs maturation and activation in osteosarcoma
These results suggest that PSK (show TAOK2 Antibodies) suppresses Hedgehog (show SHH Antibodies) signaling through down-regulation of MAML3 (show MAML3 Antibodies) and RBPJ transcription under hypoxia, inhibiting the induction of a malignant phenotype in pancreatic cancer. Our results may lead to development of new treatments for refractory pancreatic cancer using PSK (show TAOK2 Antibodies) as a Hedgehog (show SHH Antibodies) inhibitor
findings reveal that, in response to Wnt (show WNT2 Antibodies) signalling, Dishevelled (show DVL2 Antibodies) inhibits CSL (show SMPX Antibodies) transcription factors to regulate Notch (show NOTCH1 Antibodies) signalling and cell-fate decisions in vivo
The study reports the identification and functional characterization of rbpj interacting and tubulin associated (RITA) (C12ORF52 (show C12orf52 Antibodies)) as a novel rbpj/CBF-1-interacting protein.
The results suggest that a cell-to-cell interaction via the Notch (show NOTCH1 Antibodies)/Su(H) pathway has a significant role in the PGC (show PGC Antibodies) 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.
Data (including data from studies in transgenic mice) suggest that signaling via Notch2 (show NOTCH2 Antibodies) and Notch3 (show NOTCH3 Antibodies) plays role in promoting cell differentiation and steroidogenesis in preovulatory granulosa cells; mechanism involves regulation of gene expression of Jag1 (show JAG1 Antibodies) and Rbpj. (Notch2 (show NOTCH2 Antibodies) = Notch2 (show NOTCH2 Antibodies) receptor; Notch3 (show NOTCH3 Antibodies) = Notch3 (show NOTCH3 Antibodies) receptor; Jag1 (show JAG1 Antibodies) = jagged-1 (show JAG1 Antibodies) protein; Rbpj = recombining binding protein suppressor of hairless)
Macrophage maturation is controlled by Notch ligand (show JAG2 Antibodies) Dll1 (show DLL1 Antibodies) expressed in vascular endothelial cells of arteries and requires macrophage canonical Notch (show NOTCH1 Antibodies) signaling via Rbpj, which simultaneously suppresses an inflammatory macrophage fate. Conversely, conditional mutant mice lacking Dll1 (show DLL1 Antibodies) or Rbpj show proliferation and transient accumulation of inflammatory macrophages, which antagonizes arteriogenesis and tissue repair.
RBPJ binds and trans-activates the Il23r (show IL23R Antibodies) promoter and induces IL-23R (show IL23R Antibodies) expression and represses anti-inflammatory IL-10 (show IL10 Antibodies) 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 (show NOTCH1 Antibodies)/RBP-J signaling regulates dopamine responsiveness in the striatum, which may explain the mechanism whereby Notch (show NOTCH1 Antibodies)/RBP-J signaling affects an individual's susceptibility to neuropsychiatric disease.
RBP-J-mediated Notch (show NOTCH1 Antibodies) 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 (show MBD4 Antibodies) plays role in enamel formation; Med1 (show MBD4 Antibodies) induces Alpl (show ALPL Antibodies) via stimulation of Notch1 (show NOTCH1 Antibodies) signaling by forming Notch1 (show NOTCH1 Antibodies)-RBP-Jk complex on Alpl (show ALPL Antibodies) promoter. (Med1 (show MBD4 Antibodies) = mediator complex subunit 1 (show MED1 Antibodies); Alpl (show ALPL Antibodies) = alkaline phosphatase, liver-bone-kidney; Notch1 (show NOTCH1 Antibodies) = Notch gene homolog 1 (show NOTCH1 Antibodies); RBP-Jk = kappa J region recombining binding protein suppressor of hairless)
study uncovered a regulatory network, where miR (show MLXIP Antibodies)-182 functions as an important new node that receives inputs from RBP-J and TNF-alpha (show TNF Antibodies) signaling and positively regulates inflammatory osteoclastogenesis; suppression of miR (show MLXIP Antibodies)-182 by RBP-J serves as an important mechanism that restrains TNF-alpha (show TNF Antibodies) induced osteoclastogenesis
structural and biophysical studies demonstrate that RITA (show C12orf52 Antibodies) binds RBP-J similarly to the RAM (show FAM103A1 Antibodies) (RBP-J-associated molecule) domain of Notch (show NOTCH1 Antibodies), our biochemical and cellular assays suggest that RITA (show C12orf52 Antibodies) interacts with additional regions in RBP-J.
Intronic Flk1 (show KDR Antibodies) genetic enhancer element directs arterial-specific expression via RBPJ-mediated venous repression.
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.
recombining binding protein suppressor of hairless
, H-2K binding factor-2
, RBP-J kappa
, immunoglobulin kappa J region recombination signal binding protein 1
, renal carcinoma antigen NY-REN-30
, suppressor of hairless homolog
, suppressor of hairless protein 1
, suppressor of hairless protein homolog
, J kappa-recombination signal-binding protein