RBPJ Antibody

1. this report tried to address the molecular basis for the direct interaction between CSL and SMRT. PMID:30157580
2. Variants rs2270226 and rs2077777 in the RBPJ gene were associated with the risk of cerebral infarction diseases in the Chinese Han population. PMID:30075508
3. RBPJ and MAML3 could be new therapeutic targets for SCLC. PMID:30061220
4. The ULK3 Kinase Is Critical for Convergent Control of Cancer-Associated Fibroblast Activation by CSL and GLI PMID:28877478
5. 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 PMID:27489358
6. 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 PMID:27926858
7. RBPJ interacts with L3MBTL3 to promote repression of Notch signaling via histone demethylase KDM1A. PMID:29030483
8. RBPJ links MYC and transcriptional control through CDK9 in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH PMID:27322055
9. 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. PMID:28571041
10. 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. PMID:28487372
11. 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. PMID:27163456
12. RBP-J mediated by miR-133a probably contributed to the regulation of DCs maturation and activation in osteosarcoma PMID:27794430
13. 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 PMID:27466498
14. 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. PMID:26735629
15. 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. PMID:26604133
16. The role of CSL-dependent and independent Notch signaling pathways in cell apoptosis is described in normal tissue homeostasis and in tumorigenesis. (Review) PMID:26496776
17. 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. PMID:26719268
18. Suggest that hypoxia promotes SMO transcription through upregulation of MAML3 and RBPJ to induce proliferation, invasiveness and tumorigenesis in pancreatic cancer. PMID:26655998
19. data suggest that shRNA intervention of RBPJ expression could be a promising therapeutic approach for treating human prostate cancer PMID:26202358
20. Cancer-associated fibroblast activation-stromal co-evolution is under convergent CSL-p53 control. PMID:26302407
21. Single nucleotide polymorphisms in RBPJ, IL1R1, REV3L, TRAF3IP2, IRF1 and ICOS showed association with rheumatoid arthritis in black South Africans. PMID:25014791
22. missense mutations and frameshift deletions identified in leukemia patients PMID:24549417
23. Our data thus suggest that shRNA intervention of RBPJ expression could be a promising therapeutic approach for treating human lung cancer. PMID:25589461
24. RBP-J-interacting and tubulin-associated (RITA) mediates the nuclear export of RBP-J to tubulin fibers and downregulates Notch-mediated transcription. PMID:25445601
25. Data indicate that RBPJ protein depletion induces Notch target genes in a Notch-independent fashion. PMID:25512468
26. DNA methylation-dependent binding of RBPJ to a GC repressor element can negatively regulate smooth muscl myosin heavy chain promoter activity and can inhibit marker gene expression in phenotypically modulated cells PMID:25324571
27. Data suggest that, in B-lymphocytes infected with Epstein-Barr virus (EBV), EBNA3A (EBV nuclear antigen 3A) binds to CBF1-occupied intergenic enhancers located between CXCL10 and CXCL9 and displaces the transactivator EBNA2. PMID:24068939
28. KAP1, RBP-Jkappa, and HIF-1alpha play an essential role in KSHV pathogenesis. PMID:24696491
29. CBF1/CSL acts as a global hub which is used by the virus to coordinate the lytic cascade. PMID:23696732
30. Data indicate that cAMP activates Notch signaling and increases the expression of recombinant recognition sequence binding protein at the Jkappa site (RBP-J) and transducin-like enhancer of Split (TLE). PMID:23775085
31. Authors report that human papillomavirus type 8 E6 subverts NOTCH activation during keratinocyte differentiation by inhibiting RBPJ/MAML1 transcriptional activator complexes at NOTCH target DNA. PMID:23365452
32. RBPJ regulates rhabdomyosarcoma growth. PMID:22792167
33. Characterization of CSL (CBF-1, Su(H), Lag-1) mutants reveals differences in signaling mediated by Notch1 and Notch2. PMID:22915591
34. Unique mutations in RBPJ lead to impaired DNA binding in cases of Adams-Oliver syndrome. PMID:22883147
35. results indicate that PS2 modulates the degradation of RBP-Jk through phosphorylation by p38 MAPK. PMID:22302987
36. Three consensus RBP-Jkappa-binding sites found in the ORF46 promoter are critical for the binding of RBP-Jkappa protein and conferring the ORF50 responsiveness. PMID:22366521
37. Association of CSL with NICD exerts remarkably little effect on the exchange kinetics of the ANK domain, whereas MAML1 binding greatly retards the exchange kinetics of ANK repeats 2-3. PMID:22325781
38. Bacterial translocation is evident in the colonic mucosa of transgenic RBP-J(DeltaIEC) mice before the onset of colitis, suggesting attenuated epithelial barrier functions in these mice. PMID:22279105
39. RBP-Jkappa binding sites within the RTA promoter regulate KSHV latent infection and cell proliferation. PMID:22253595
40. RBP-J binds methylated DNA in the context of a mutated RBP-J consensus motif. PMID:21991380
41. DNA binding and tetramerization mutants of Rta fail to stimulate RBP-Jk binding to Kaposi's sarcoma-associated herpesvirus DNA. PMID:21880753
42. there is a conserved network of cis-regulatory factors that interacts with Notch1 to regulate gene expression in TLL cells, as well as unique classes of divergent RBPJ-only sites that also likely regulate transcription PMID:21737748
43. Collectively, our results demonstrate that APP intracellular domain functions as a negative regulator in Notch1 signaling through the promotion of Notch1 and RBP-Jk protein degradation PMID:21558417
44. The RBP-Jkappa binding site within the KSHV LANA promoter is crucial for HHV8 latency during early primary infection. PMID:21507979
45. These results indicate that EBNA3 proteins interact with multiple RBP/CSL domains, but only N-terminal domain interactions are required for lymphoblastoid cell line growth. PMID:21440926
46. data strongly support a model in which EBNA2 association with NCoR-deficient RBPJ enhances transcription and EBNALP dismisses NCoR and RBPJ repressive complexes from enhancers PMID:21518914
47. Notch target gene activator RBP-J kappa transgene plays no role in Notch target gene repression in Ikaros double-positive thymocytes during leukemia development. PMID:20511547
48. mechanism by which the PhiW PhiP motif of RAM and EBNA2 compete with one another for binding at the hydrophobic pocket of the beta-trefoil domain (BTD) of CSL using overlapping but specific interactions that are unique to each BTD ligand. PMID:20028974
49. Studies indicate that the mechanisms that lead to Notch activity in the receiving cell include the cleavage of Notch at the cell membrane and the assembly of a nuclear complex with the transcription factors CSL. PMID:19247952
50. The interactions of RBPJ with ORF47 and ORF50 human herpesvirus 8 proteins in transactivation are reported. PMID:20006367

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HGNC: 5724

UNIGENE: Hs.479396

KEGG: hsa:3516

STRING: 9606.ENSP00000345206

OMIM: 147183