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We show that GIT1, which also contains an ANK domain, inhibits the Notch1 (show NOTCH1 Proteins)-Dll4 (show DLL4 Proteins) signaling pathway by competing with Notch1 (show NOTCH1 Proteins) ANK domain for binding to RBP-J in stalk cells
we report that genetic removal of CSL (show CSHL1 Proteins) in breast tumor cells caused accelerated growth of xenografted tumors. Loss of CSL (show CSHL1 Proteins) unleashed a hypoxic response during normoxic conditions, manifested by stabilization of the HIF1alpha (show HIF1A Proteins) protein and acquisition of a polyploid giant-cell, cancer stem cell-like, phenotype.
RBPJ interacts with L3MBTL3 (show L3MBTL3 Proteins) to promote repression of Notch (show NOTCH1 Proteins) signaling via histone demethylase (show MBD2 Proteins) KDM1A (show KDM1A Proteins).
RBPJ links MYC (show MYC Proteins) and transcriptional control through CDK9 (show CDK9 Proteins) in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH (show NOTCH1 Proteins)
Mean CBF1 expression is significantly increased in isocitrate dehydrogenase 1 (IDH1 (show IDH1 Proteins)) 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 Proteins) binds RBP-J similarly to the RAM (show RAB27A Proteins) (RBP-J-associated molecule) domain of Notch (show NOTCH1 Proteins), our biochemical and cellular assays suggest that RITA (show ZNF331 Proteins) interacts with additional regions in RBP-J.
The present findings indicate that p53 (show TP53 Proteins), in turn, decreases CSL (show CSHL1 Proteins) expression, which can serve to enhance p53 (show TP53 Proteins) activity in acute DNA damage response of cells.
RBP-J mediated by miR (show MLXIP Proteins)-133a probably contributed to the regulation of DCs maturation and activation in osteosarcoma
These results suggest that PSK (show TAOK2 Proteins) suppresses Hedgehog (show SHH Proteins) signaling through down-regulation of MAML3 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 Proteins) as a Hedgehog (show SHH Proteins) inhibitor
our findings reconcile the 2 biological events and point to a multistep process of CAF (show KAT2B Proteins) activation under convergent CSL (show CSHL1 Proteins) and p53 (show TP53 Proteins) control. Activation of p53 (show TP53 Proteins) provides a failsafe mechanism against consequences of compromised CSL (show CSHL1 Proteins) activity in stromal cells.
findings reveal that, in response to Wnt (show WNT2 Proteins) signalling, Dishevelled (show DVL2 Proteins) inhibits CSL (show SMPX Proteins) transcription factors to regulate Notch (show NOTCH1 Proteins) 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 Proteins)) as a novel rbpj/CBF-1-interacting protein.
The results suggest that a cell-to-cell interaction via the Notch (show NOTCH1 Proteins)/Su(H) pathway has a significant role in the PGC (show PGC Proteins) 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.
Macrophage maturation is controlled by Notch ligand (show JAG2 Proteins) Dll1 (show DLL1 Proteins) expressed in vascular endothelial cells of arteries and requires macrophage canonical Notch (show NOTCH1 Proteins) signaling via Rbpj, which simultaneously suppresses an inflammatory macrophage fate. Conversely, conditional mutant mice lacking Dll1 (show DLL1 Proteins) 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 Proteins) promoter and induces IL-23R (show IL23R Proteins) expression and represses anti-inflammatory IL-10 (show IL10 Proteins) 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 Proteins)/RBP-J signaling regulates dopamine responsiveness in the striatum, which may explain the mechanism whereby Notch (show NOTCH1 Proteins)/RBP-J signaling affects an individual's susceptibility to neuropsychiatric disease.
RBP-J-mediated Notch (show NOTCH1 Proteins) 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 Proteins) plays role in enamel formation; Med1 (show MBD4 Proteins) induces Alpl (show ALPL Proteins) via stimulation of Notch1 (show NOTCH1 Proteins) signaling by forming Notch1 (show NOTCH1 Proteins)-RBP-Jk complex on Alpl (show ALPL Proteins) promoter. (Med1 (show MBD4 Proteins) = mediator complex subunit 1 (show MED1 Proteins); Alpl (show ALPL Proteins) = alkaline phosphatase, liver-bone-kidney; Notch1 (show NOTCH1 Proteins) = Notch gene homolog 1 (show NOTCH1 Proteins); RBP-Jk = kappa J region recombining binding protein suppressor of hairless)
study uncovered a regulatory network, where miR (show MLXIP Proteins)-182 functions as an important new node that receives inputs from RBP-J and TNF-alpha (show TNF Proteins) signaling and positively regulates inflammatory osteoclastogenesis; suppression of miR (show MLXIP Proteins)-182 by RBP-J serves as an important mechanism that restrains TNF-alpha (show TNF Proteins) induced osteoclastogenesis
structural and biophysical studies demonstrate that RITA (show C12orf52 Proteins) binds RBP-J similarly to the RAM (show FAM103A1 Proteins) (RBP-J-associated molecule) domain of Notch (show NOTCH1 Proteins), our biochemical and cellular assays suggest that RITA (show C12orf52 Proteins) interacts with additional regions in RBP-J.
Intronic Flk1 (show KDR Proteins) genetic enhancer element directs arterial-specific expression via RBPJ-mediated venous repression.
Rbpj-kappa mediated Notch (show NOTCH1 Proteins) signaling plays a critical role in development of hypothalamic Kisspeptin neurons.
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