Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Rat (Rattus) RBPJ Antibodies:
anti-Human RBPJ Antibodies:
anti-Mouse (Murine) RBPJ Antibodies:
Go to our pre-filtered search.
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
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
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
our findings reconcile the 2 biological events and point to a multistep process of CAF (show KAT2B Antibodies) activation under convergent CSL (show CSHL1 Antibodies) and p53 (show TP53 Antibodies) control. Activation of p53 (show TP53 Antibodies) provides a failsafe mechanism against consequences of compromised CSL (show CSHL1 Antibodies) activity in stromal cells.
RBPJ polymorphism [rs874040(CC) allele] skews memory T cells toward a pro-inflammatory phenotype involving Notch (show NOTCH1 Antibodies) signaling, thus increasing the susceptibility to develop rheumatoid arthritis.
The role of CSL (show CSHL1 Antibodies)-dependent and independent Notch (show NOTCH1 Antibodies) signaling pathways in cell apoptosis is described in normal tissue homeostasis and in tumorigenesis. (Review)
These results support a model in which EBNA2 and EBNA3s compete for distinct subsets of RBPJ sites to regulate cell genes and where EBNA3 (show EBNA-3A Antibodies) subset specificity is determined by interactions with other cell transcription factors.
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.
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.
Rbpj-kappa mediated Notch (show NOTCH1 Antibodies) signaling plays a critical role in development of hypothalamic Kisspeptin neurons.
Results reveal an essential role for canonical Notch (show NOTCH1 Antibodies)/RBP-J signaling in hippocampal synaptic plasticity and suggest that role, at least in part, is mediated by the regulation of GABAergic signaling
The bone marrow contains a progenitor that expresses renin (show REN Antibodies) throughout development and possesses a B-lymphocyte (show AKAP17A Antibodies) pedigree. This cell requires RBP-J to differentiate.
functions as a transcriptional repressor on the promoter of the microRNA miR (show MLXIP Antibodies)-155
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