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