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The DNA-binding protein CSL is the centrepiece of transcriptional regulation in the Notch pathway, acting as a molecular hub for interactions with either corepressors or coactivators to repress or activate, respectively, transcription.
data, taken together, indicate that RBPJ regulates inflammation during endometrial repair, which is essential for future pregnancy potential, and its dysregulation may serve as an unidentified contributor to unexplained recurrent pregnancy loss.
this report tried to address the molecular basis for the direct interaction between CSL and SMRT.
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 could be new therapeutic targets for SCLC.
The ULK3 Kinase Is Critical for Convergent Control of Cancer-Associated Fibroblast Activation by CSL and GLI
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 domain, inhibits the Notch1-Dll4 signaling pathway by competing with Notch1 ANK domain for binding to RBP-J in stalk cells
we report that genetic removal of CSL in breast tumor cells caused accelerated growth of xenografted tumors. Loss of CSL unleashed a hypoxic response during normoxic conditions, manifested by stabilization of the HIF1alpha protein and acquisition of a polyploid giant-cell, cancer stem cell-like, phenotype.
RBPJ interacts with L3MBTL3 to promote repression of Notch signaling via histone demethylase KDM1A.
RBPJ links MYC and transcriptional control through CDK9 in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH
Mean CBF1 expression is significantly increased in isocitrate dehydrogenase 1 (IDH1) 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 binds RBP-J similarly to the RAM (RBP-J-associated molecule) domain of Notch, our biochemical and cellular assays suggest that RITA interacts with additional regions in RBP-J.
The present findings indicate that p53, in turn, decreases CSL expression, which can serve to enhance p53 activity in acute DNA damage response of cells.
RBP-J mediated by miR-133a probably contributed to the regulation of DCs maturation and activation in osteosarcoma
These results suggest that PSK suppresses Hedgehog 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 as a Hedgehog inhibitor
our findings reconcile the 2 biological events and point to a multistep process of CAF activation under convergent CSL and p53 control. Activation of p53 provides a failsafe mechanism against consequences of compromised CSL activity in stromal cells.
RBPJ polymorphism [rs874040(CC) allele] skews memory T cells toward a pro-inflammatory phenotype involving Notch signaling, thus increasing the susceptibility to develop rheumatoid arthritis.
The role of CSL-dependent and independent Notch 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 subset specificity is determined by interactions with other cell transcription factors.
Sca1(+)Lin(-)CD117(-) mouse bone marrow-derived mesenchymal stem cells regulate immature dendritic cell maturation by inhibiting TLR4-IRF8 signaling via the Notch-RBP-J pathway.
findings show that the RBP-J-mediated Notch signaling pathway in cardiomyocytes limits ventricular remodeling and improves cardiac function after MI. The RBP-J-mediated Notch signaling pathway has a protective role in cardiomyocyte apoptosis following cardiac injury.
homoeostatic repressor of multiple pro-angiogenic and angiostatic factor genes in cardiomyocytes
Early pancreatic islet fate and maturation is controlled through RBP-Jkappa.
In this study, the authors found that conditional disruption of RBP-J, the transcription factor of canonical Notch signaling, increased irradiation sensitivity in mice.
Data (including data from studies in transgenic mice) suggest that signaling via Notch2 and Notch3 plays role in promoting cell differentiation and steroidogenesis in preovulatory granulosa cells; mechanism involves regulation of gene expression of Jag1 and Rbpj. (Notch2 = Notch2 receptor; Notch3 = Notch3 receptor; Jag1 = jagged-1 protein; Rbpj = recombining binding protein suppressor of hairless)
Macrophage maturation is controlled by Notch ligand Dll1 expressed in vascular endothelial cells of arteries and requires macrophage canonical Notch signaling via Rbpj, which simultaneously suppresses an inflammatory macrophage fate. Conversely, conditional mutant mice lacking Dll1 or Rbpj show proliferation and transient accumulation of inflammatory macrophages, which antagonizes arteriogenesis and tissue repair.
RBPJ binds and trans-activates the Il23r promoter and induces IL-23R expression and represses anti-inflammatory IL-10 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/RBP-J signaling regulates dopamine responsiveness in the striatum, which may explain the mechanism whereby Notch/RBP-J signaling affects an individual's susceptibility to neuropsychiatric disease.
RBP-J-mediated Notch 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 plays role in enamel formation; Med1 induces Alpl via stimulation of Notch1 signaling by forming Notch1-RBP-Jk complex on Alpl promoter. (Med1 = mediator complex subunit 1; Alpl = alkaline phosphatase, liver-bone-kidney; Notch1 = Notch gene homolog 1; RBP-Jk = kappa J region recombining binding protein suppressor of hairless)
study uncovered a regulatory network, where miR-182 functions as an important new node that receives inputs from RBP-J and TNF-alpha signaling and positively regulates inflammatory osteoclastogenesis; suppression of miR-182 by RBP-J serves as an important mechanism that restrains TNF-alpha induced osteoclastogenesis
Intronic Flk1 genetic enhancer element directs arterial-specific expression via RBPJ-mediated venous repression.
Rbpj-kappa mediated Notch signaling plays a critical role in development of hypothalamic Kisspeptin neurons.
Results reveal an essential role for canonical Notch/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 throughout development and possesses a B-lymphocyte pedigree. This cell requires RBP-J to differentiate.
functions as a transcriptional repressor on the promoter of the microRNA miR-155
findings reveal that, in response to Wnt signalling, Dishevelled inhibits CSL transcription factors to regulate Notch signalling and cell-fate decisions in vivo
The study reports the identification and functional characterization of rbpj interacting and tubulin associated (RITA) (C12ORF52) as a novel rbpj/CBF-1-interacting protein.
The results suggest that a cell-to-cell interaction via the Notch/Su(H) pathway has a significant role in the PGC 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.
embryos treated with morpholinos against wt1a, foxc1a, or the Notch transcriptional mediator rbpj develop fewer podocytes, as determined by wt1b, hey1 and nephrin expression, while embryos deficient in any two of these factors completely lack podocytes
her8a is positively regulated by Su(H)-dependent Notch signaling as revealed by a Notch-defective mutant and injection of variants of the Notch intracellular regulator, Su(H).
analysed the function of Su(H) in the somitogenesis process and its influence on the expression of notch pathway genes
one element of the Notch 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