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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 (Montrer ULK3 Protéines) Kinase Is Critical for Convergent Control of Cancer-Associated Fibroblast Activation by CSL (Montrer CSHL1 Protéines) and GLI (Montrer GLI1 Protéines)
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 (Montrer NOTCH1 Protéines)-Dll4 (Montrer DLL4 Protéines) signaling pathway by competing with Notch1 (Montrer NOTCH1 Protéines) ANK domain for binding to RBP-J in stalk cells
we report that genetic removal of CSL (Montrer CSHL1 Protéines) in breast tumor cells caused accelerated growth of xenografted tumors. Loss of CSL (Montrer CSHL1 Protéines) unleashed a hypoxic response during normoxic conditions, manifested by stabilization of the HIF1alpha (Montrer HIF1A Protéines) protein and acquisition of a polyploid giant-cell, cancer stem cell-like, phenotype.
RBPJ interacts with L3MBTL3 (Montrer L3MBTL3 Protéines) to promote repression of Notch (Montrer NOTCH1 Protéines) signaling via histone demethylase (Montrer MBD2 Protéines) KDM1A (Montrer KDM1A Protéines).
RBPJ links MYC (Montrer MYC Protéines) and transcriptional control through CDK9 (Montrer CDK9 Protéines) in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH (Montrer NOTCH1 Protéines)
Mean CBF1 expression is significantly increased in isocitrate dehydrogenase 1 (IDH1 (Montrer IDH1 Protéines)) 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 (Montrer ZNF331 Protéines) binds RBP-J similarly to the RAM (Montrer RAB27A Protéines) (RBP-J-associated molecule) domain of Notch (Montrer NOTCH1 Protéines), our biochemical and cellular assays suggest that RITA (Montrer ZNF331 Protéines) interacts with additional regions in RBP-J.
Early pancreatic islet fate and maturation is controlled through RBP (Montrer RBP4 Protéines)-Jkappa.
In this study, the authors found that conditional disruption of RBP-J, the transcription factor of canonical Notch (Montrer NOTCH1 Protéines) signaling, increased irradiation sensitivity in mice.
Data (including data from studies in transgenic mice) suggest that signaling via Notch2 (Montrer NOTCH2 Protéines) and Notch3 (Montrer NOTCH3 Protéines) plays role in promoting cell differentiation and steroidogenesis in preovulatory granulosa cells; mechanism involves regulation of gene expression of Jag1 (Montrer JAG1 Protéines) and Rbpj. (Notch2 (Montrer NOTCH2 Protéines) = Notch2 (Montrer NOTCH2 Protéines) receptor; Notch3 (Montrer NOTCH3 Protéines) = Notch3 (Montrer NOTCH3 Protéines) receptor; Jag1 (Montrer JAG1 Protéines) = jagged-1 (Montrer JAG1 Protéines) protein; Rbpj = recombining binding protein suppressor of hairless)
Macrophage maturation is controlled by Notch ligand (Montrer JAG2 Protéines) Dll1 (Montrer DLL1 Protéines) expressed in vascular endothelial cells of arteries and requires macrophage canonical Notch (Montrer NOTCH1 Protéines) signaling via Rbpj, which simultaneously suppresses an inflammatory macrophage fate. Conversely, conditional mutant mice lacking Dll1 (Montrer DLL1 Protéines) or Rbpj show proliferation and transient accumulation of inflammatory macrophages, which antagonizes arteriogenesis and tissue repair.
RBPJ binds and trans-activates the Il23r (Montrer IL23R Protéines) promoter and induces IL-23R (Montrer IL23R Protéines) expression and represses anti-inflammatory IL-10 (Montrer IL10 Protéines) 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 (Montrer NOTCH1 Protéines)/RBP-J signaling regulates dopamine responsiveness in the striatum, which may explain the mechanism whereby Notch (Montrer NOTCH1 Protéines)/RBP-J signaling affects an individual's susceptibility to neuropsychiatric disease.
RBP-J-mediated Notch (Montrer NOTCH1 Protéines) 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 (Montrer MBD4 Protéines) plays role in enamel formation; Med1 (Montrer MBD4 Protéines) induces Alpl (Montrer ALPL Protéines) via stimulation of Notch1 (Montrer NOTCH1 Protéines) signaling by forming Notch1 (Montrer NOTCH1 Protéines)-RBP-Jk complex on Alpl (Montrer ALPL Protéines) promoter. (Med1 (Montrer MBD4 Protéines) = mediator complex subunit 1 (Montrer MED1 Protéines); Alpl (Montrer ALPL Protéines) = alkaline phosphatase, liver-bone-kidney; Notch1 (Montrer NOTCH1 Protéines) = Notch gene homolog 1 (Montrer NOTCH1 Protéines); RBP-Jk = kappa J region recombining binding protein suppressor of hairless)
study uncovered a regulatory network, where miR (Montrer MLXIP Protéines)-182 functions as an important new node that receives inputs from RBP-J and TNF-alpha (Montrer TNF Protéines) signaling and positively regulates inflammatory osteoclastogenesis; suppression of miR (Montrer MLXIP Protéines)-182 by RBP-J serves as an important mechanism that restrains TNF-alpha (Montrer TNF Protéines) induced osteoclastogenesis
structural and biophysical studies demonstrate that RITA (Montrer C12orf52 Protéines) binds RBP-J similarly to the RAM (Montrer FAM103A1 Protéines) (RBP-J-associated molecule) domain of Notch (Montrer NOTCH1 Protéines), our biochemical and cellular assays suggest that RITA (Montrer C12orf52 Protéines) interacts with additional regions in RBP-J.
findings reveal that, in response to Wnt (Montrer WNT2 Protéines) signalling, Dishevelled (Montrer DVL2 Protéines) inhibits CSL (Montrer SMPX Protéines) transcription factors to regulate Notch (Montrer NOTCH1 Protéines) signalling and cell-fate decisions in vivo
The study reports the identification and functional characterization of rbpj interacting and tubulin associated (RITA) (C12ORF52 (Montrer C12orf52 Protéines)) as a novel rbpj/CBF-1-interacting protein.
The results suggest that a cell-to-cell interaction via the Notch (Montrer NOTCH1 Protéines)/Su(H) pathway has a significant role in the PGC (Montrer PGC Protéines) 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.
Intronic Flk1 (Montrer KDR Protéines) genetic enhancer element directs arterial-specific expression via RBPJ-mediated venous repression.
embryos treated with morpholinos against wt1a, foxc1a, or the Notch (Montrer NOTCH1 Protéines) transcriptional mediator rbpj develop fewer podocytes, as determined by wt1b (Montrer WT1 Protéines), hey1 (Montrer HEY1 Protéines) and nephrin (Montrer NPHS1 Protéines) expression, while embryos deficient in any two of these factors completely lack podocytes
her8a is positively regulated by Su(H)-dependent Notch (Montrer NOTCH1 Protéines) signaling as revealed by a Notch (Montrer NOTCH1 Protéines)-defective mutant and injection of variants of the Notch (Montrer NOTCH1 Protéines) intracellular regulator, Su(H).
analysed the function of Su(H) in the somitogenesis process and its influence on the expression of notch (Montrer NOTCH1 Protéines) pathway genes
one element of the Notch (Montrer NOTCH1 Protéines) 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