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We show that GIT1, which also contains an ANK (显示 ANK1 ELISA试剂盒) domain, inhibits the Notch1 (显示 NOTCH1 ELISA试剂盒)-Dll4 (显示 DLL4 ELISA试剂盒) signaling pathway by competing with Notch1 (显示 NOTCH1 ELISA试剂盒) ANK (显示 ANK1 ELISA试剂盒) 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 (显示 HIF1A ELISA试剂盒) protein and acquisition of a polyploid giant-cell, cancer stem cell-like, phenotype.
RBPJ interacts with L3MBTL3 to promote repression of Notch (显示 NOTCH1 ELISA试剂盒) signaling via histone demethylase (显示 MBD2 ELISA试剂盒) KDM1A (显示 KDM1A ELISA试剂盒).
RBPJ links MYC (显示 MYC ELISA试剂盒) and transcriptional control through CDK9 (显示 CDK9 ELISA试剂盒) in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH (显示 NOTCH1 ELISA试剂盒)
Mean CBF1 expression is significantly increased in isocitrate dehydrogenase 1 (IDH1 (显示 IDH1 ELISA试剂盒)) 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 ELISA试剂盒) binds RBP-J similarly to the RAM (显示 RAB27A ELISA试剂盒) (RBP-J-associated molecule) domain of Notch (显示 NOTCH1 ELISA试剂盒), our biochemical and cellular assays suggest that RITA (显示 ZNF331 ELISA试剂盒) interacts with additional regions in RBP-J.
The present findings indicate that p53 (显示 TP53 ELISA试剂盒), in turn, decreases CSL expression, which can serve to enhance p53 (显示 TP53 ELISA试剂盒) activity in acute DNA damage response of cells.
RBP-J mediated by miR (显示 MLXIP ELISA试剂盒)-133a probably contributed to the regulation of DCs maturation and activation in osteosarcoma
These results suggest that PSK (显示 TAOK2 ELISA试剂盒) suppresses Hedgehog (显示 SHH ELISA试剂盒) 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 (显示 TAOK2 ELISA试剂盒) as a Hedgehog (显示 SHH ELISA试剂盒) inhibitor
our findings reconcile the 2 biological events and point to a multistep process of CAF (显示 KAT2B ELISA试剂盒) activation under convergent CSL and p53 (显示 TP53 ELISA试剂盒) control. Activation of p53 (显示 TP53 ELISA试剂盒) provides a failsafe mechanism against consequences of compromised CSL activity in stromal cells.
findings reveal that, in response to Wnt (显示 WNT2 ELISA试剂盒) signalling, Dishevelled (显示 DVL2 ELISA试剂盒) inhibits CSL (显示 SMPX ELISA试剂盒) transcription factors to regulate Notch (显示 NOTCH1 ELISA试剂盒) 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 ELISA试剂盒)) as a novel rbpj/CBF-1-interacting protein.
The results suggest that a cell-to-cell interaction via the Notch (显示 NOTCH1 ELISA试剂盒)/Su(H) pathway has a significant role in the PGC (显示 PGC ELISA试剂盒) 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.
RBPJ binds and trans-activates the Il23r (显示 IL23R ELISA试剂盒) promoter and induces IL-23R (显示 IL23R ELISA试剂盒) expression and represses anti-inflammatory IL-10 (显示 IL10 ELISA试剂盒) 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 ELISA试剂盒)/RBP-J signaling regulates dopamine responsiveness in the striatum, which may explain the mechanism whereby Notch (显示 NOTCH1 ELISA试剂盒)/RBP-J signaling affects an individual's susceptibility to neuropsychiatric disease.
RBP-J-mediated Notch (显示 NOTCH1 ELISA试剂盒) 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 ELISA试剂盒) plays role in enamel formation; Med1 (显示 MBD4 ELISA试剂盒) induces Alpl (显示 ALPL ELISA试剂盒) via stimulation of Notch1 (显示 NOTCH1 ELISA试剂盒) signaling by forming Notch1 (显示 NOTCH1 ELISA试剂盒)-RBP-Jk complex on Alpl (显示 ALPL ELISA试剂盒) promoter. (Med1 (显示 MBD4 ELISA试剂盒) = mediator complex subunit 1 (显示 MED1 ELISA试剂盒); Alpl (显示 ALPL ELISA试剂盒) = alkaline phosphatase, liver-bone-kidney; Notch1 (显示 NOTCH1 ELISA试剂盒) = Notch gene homolog 1 (显示 NOTCH1 ELISA试剂盒); RBP-Jk = kappa J region recombining binding protein suppressor of hairless)
study uncovered a regulatory network, where miR (显示 MLXIP ELISA试剂盒)-182 functions as an important new node that receives inputs from RBP-J and TNF-alpha (显示 TNF ELISA试剂盒) signaling and positively regulates inflammatory osteoclastogenesis; suppression of miR (显示 MLXIP ELISA试剂盒)-182 by RBP-J serves as an important mechanism that restrains TNF-alpha (显示 TNF ELISA试剂盒) induced osteoclastogenesis
structural and biophysical studies demonstrate that RITA (显示 C12orf52 ELISA试剂盒) binds RBP-J similarly to the RAM (RBP-J-associated molecule) domain of Notch (显示 NOTCH1 ELISA试剂盒), our biochemical and cellular assays suggest that RITA (显示 C12orf52 ELISA试剂盒) interacts with additional regions in RBP-J.
Intronic Flk1 (显示 KDR ELISA试剂盒) genetic enhancer element directs arterial-specific expression via RBPJ-mediated venous repression.
Rbpj-kappa mediated Notch (显示 NOTCH1 ELISA试剂盒) signaling plays a critical role in development of hypothalamic Kisspeptin neurons.
Results reveal an essential role for canonical Notch (显示 NOTCH1 ELISA试剂盒)/RBP-J signaling in hippocampal synaptic plasticity and suggest that role, at least in part, is mediated by the regulation of GABAergic signaling
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