RELB Antibody

1. Results show that GSK3beta modulates RelB degradation. PMID:29358699
2. Data show that TNF receptor-associated factor 3 (TRAF3) autophagy is driven by RAS and results in activation of transcription factor RelB (RELB). PMID:29146913
3. TNF-alpha-induced expression of transport protein genes in HUVEC cells is associated with enhanced expression of RELB and NFKB2. PMID:29658079
4. results suggest that changes in the relative concentrations of RelB, NIK:IKK1, and p100 during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100. PMID:27678221
5. Low RELB expression is associated with Prostate Cancer. PMID:28108513
6. RelB is processed by CO2 in a manner dependent on a key C-terminal domain located in its transactivation domain. Loss of the RelB transactivation domain alters NF-kappaB-dependent transcriptional activity, and loss of p100 alters sensitivity of RelB to CO2 PMID:28507099
7. EZH2, through a methyltransferase-independent mechanism, promotes the transcriptional activation of the non-canonical NF-kappaB subunit RelB PMID:27764181
8. The altered expression of anti-apoptotic gene Bcl-2 played critical roles in regulating both spontaneous and radiation-induced apoptosis in the presence of RelB knockdown. For the first time, we showed that RelB knockdown significantly attenuated the migration and invasion of DU145 prostate cancer cells, due to the reduction of integrin b-1 PMID:27121503
9. Knockdown of ADGRG2 breast cancer cell lines resulted in a strong reduction in cell adhesion and subsequent cell migration which was associated with a selective reduction in RelB. PMID:26321231
10. the role of RelB on lymphocyte development in humans was shown. PMID:26385063
11. In conclusion, DECs show a unique hypo-responsive phenotype to the pro-inflammatory stimulus LPS in order to control the inflammatory response at feto-maternal interface. PMID:26463648
12. Lung-specific (CC-16) and novel (RelB) biomarkers are associated with systemic cardiovascular changes over time. PMID:26914709
13. results suggest that glucocorticoids induce a transcription complex consisting of RelB/p52, CBP, and HDAC1 that triggers a dynamic acetylation-mediated epigenetic change to induce CRH expression in full-term human placenta. PMID:26307012
14. HDAC4-RelB-p52 complex maintains repressive chromatin around proapoptotic genes Bim and BMF and regulates multiple myeloma survival and growth PMID:26455434
15. RELB enhances proliferation of human-induced pluripotent stem cells without affecting their pluripotency. RELB interacts with LIN28A and IMP3. PMID:25794352
16. In non-small cell lung cancer, RelB expression was identified in proliferating tumor cells. tumor RelB expression was an independent predictor of lymph node metastasis PMID:26147201
17. Basal expression of RelB was significantly lower in lung cells derived from smokers with and without COPD. PMID:25943190
18. RelB may represent a novel marker of health outcomes PMID:25409035
19. the specific Asp205 cleavage of RelB by caspase-3 would be involved in the apoptosis induction by anticancer agents, which would provide the positive feedback mechanism. PMID:25511695
20. we demonstrate that SUMOylation of RelB might be one of these post-translational modifications rendering the function of the NF-kappaB transcription factor RelB. PMID:24616021
21. RelB-p52 dimers were found to directly bind to the IDO promoter, leading to IDO expression in MDSCs PMID:25063873
22. Unstimulated monocyte-derived dendritic cells express RelB at low level, However, RelB increases, following stimulation, are attenuated by geldanamycin. PMID:24524692
23. CTNNA1 expression is specifically downregulated in basal-like breast cancer subtype, correlates with clinical outcome and inversely correlates with TNF and RELB expression. PMID:24509793
24. The NF-kappaB protein RelB is expressed in a particularly aggressive mesenchymal subtype of glioma. PMID:23451236
25. RelB activation is key for promoting multiple myeloma cell survival through the upregulation of anti-apoptotic proteins, in particular, CIAP2. PMID:23555623
26. The dimer RelB/p50 rather than the p50/p50 complex inhibits TNF production in lipopolysaccharide-stimulated dendritic cells and macrophages. PMID:23394901
27. a novel link between NF-kappaB and growth-inhibitory pathways involving the RelB-dependent transcriptional upregulation of p53. PMID:22777360
28. Kaposi's sarcoma-associated herpesvirus oncoprotein K13 upregulated the expression of NF-kappaB subunit RelB and blocked the anti-IgM-induced decline in c-Myc and rise in p27(Kip1) that have been associated with growth arrest and apoptosis. PMID:23236068
29. The expression of RelB negatively regulates the endogenous expression of maspin in prostate cancer cells in vitro. PMID:22780967
30. The RelB subunit of NFkappaB acts as a negative regulator of circadian gene expression. PMID:22894897
31. These data show that Hodgkin lymphoma is uniquely dependent on relB PMID:22968463
32. RelB/NF-kappaB2, is constitutively activated in the human placenta, which binds to a previously undescribed NF-kappaB enhancer of corticotropin-releasing hormone (CRH) gene promoter to regulate CRH expression. PMID:22734038
33. RelB is a CO(2)-sensitive NF-kappaB family member that may contribute to the beneficial effects of hypercapnia in inflammatory diseases of the lung PMID:22396550
34. RelB plays a critical role in the response of PCa to radiotherapy and the inverse expression of IL-8 and PSA PMID:22403723
35. We propose that RelB is an essential molecule controlling the endogenous and the proteasome inhibitor-induced Maspin expression. PMID:21856005
36. a central role for Malt1-dependent RelB cleavage in canonical NF-kappaB activation and thereby provide a rationale for the targeting of Malt1 in immunomodulation and cancer treatment. PMID:21873235
37. AHR overexpression is found among estrogen receptor (ER)alpha-negative human breast tumors and that its overexpression is positively correlated to that of the NF-kappaB subunit Rel-B and Interleukin 8. PMID:21640702
38. Data show that RelB is inducibly phosphorylated by GSK-3beta, indicating a direct substrate-enzyme relationship. PMID:21217772
39. epigenetic RELB silencing as a new marker of the progressive disease in males PMID:21062507
40. Bovine foamy virus transactivator BTas interacts with cellular RelB to enhance viral transcription. PMID:20844054
41. REQ functions as an efficient adaptor protein between the SWI/SNF complex and RelB/p52 and plays important roles in noncanonical NF-kappaB transcriptional activation and its associated oncogenic activity. PMID:20460684
42. the Tio oncoprotein triggers noncanonical NF-kappaB signaling through NEMO-dependent up-regulation of p100 precursor and RelB, as well as through NEMO-independent generation of p52 effector PMID:20353939
43. the results suggest that RelB was responsible for the LPS-mediated attachment and may play an important role in the progression of some cancers. PMID:19903458
44. Rel activity plays role in regulation of apoptosis in hepatocellular carcinoma through activation of downstream target genes PMID:12365017
45. During dendritic cell maturation, rapidly activated dimers (e.g., RelA) bound to a subset of target promoters are gradually replaced by slowly activated dimers (e.g., RelB). PMID:12820969
46. RelB has an effect on p100 processing, which is possibly regulated in a signal-dependent manner PMID:12874295
47. RelB mediates TNF-induced up-regulation of the human polymeric Ig receptor. PMID:15265917
48. RelB overexpression promoted, whereas endogenous RelB inhibition (by p100DeltaN) blocked, precursor cell development along this DC subset pathway. PMID:15315978
49. induced by cytomegalovirus (CMV) immediate-early 1 protein via activation of JNK and AP-1 PMID:15596805
50. RelB expression during dendritic cells differentiation is controlled by protein kinase CbetaII-mediated regulation of transcriptional initiation and elongation PMID:16107733

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HGNC: 9956

UNIGENE: Hs.654402

KEGG: hsa:5971

STRING: 9606.ENSP00000221452

OMIM: 604758