• Transcription factor RelB is a protein that in humans is encoded by the RELB gene. (wikipedia.org)
  • These analyses suggest that an integrated NF-κB system network underlies activation of both RelA and RelB containing dimer and that a malfunctioning canonical pathway will lead to an aberrant cellular response also through the non-canonical pathway. (wikipedia.org)
  • To examine NF-κB RelB signaling in DCs inside a quantitative way we created a numerical model that identifies the development and rules of RelA and RelB dimers with regards to mass actions kinetics (Supplementary Records). (buyresearchchemicalss.net)
  • Moreover, generation of canonical and non-canonical dimers, viz RelA:p50 and RelB:p52, within the cellular milieu are mechanistically interlinked. (wikipedia.org)
  • In resting cells, RelB is sequestered by the NF-κB precursor protein p100 in the cytoplasm. (wikipedia.org)
  • In this pathway, NIK stimulates the processing of p100 into p52, which in association with RelB appears in the nucleus as RelB:p52 NF-κB heterodimers. (wikipedia.org)
  • these together potently accumulated unprocessed p100, which attenuated the RelB activity. (wikipedia.org)
  • The non-canonical pathway involving the kinases NIK and IKK1 triggers processing of p100 to p52 and generation of the RelB-p52 transcription factor which is implicated in cell survival and maturation. (buyresearchchemicalss.net)
  • p100 encoded from the gene may inhibit RelB. (buyresearchchemicalss.net)
  • We consequently examined if p100 manifestation correlated with improved RelB manifestation in BMDCs. (buyresearchchemicalss.net)
  • For example, syntheses of the constituents of the non-canonical pathway, viz RelB and p52, are controlled by canonical IKK2-IκB-RelA:p50 signalling. (wikipedia.org)
  • RelB was also found to be rapidly triggered in DCs by canonical pathway stimuli TNF and lipopolysaccharide (LPS)16-19 and the canonical signaling pathway component TRAF6 was shown to be essential9. (buyresearchchemicalss.net)
  • We used a Systems Biology approach of iterative computational modeling and quantitative experimental analyses of the NF-κB signaling network in DCs to reveal that RelB activity was limited by classical IκBs IκBα and IκBε and regulated via the canonical pathway. (buyresearchchemicalss.net)
  • Modeling studies identified two DC-specific control points that render RelB subject to regulation by the canonical pathway and we demonstrated their sufficiency by engineering MEFs accordingly to produce Cyclo (-RGDfK) DC-like RelB control. (buyresearchchemicalss.net)
  • Finally gene expression profiling revealed that RelB-dependent gene expression programs regulated by the canonical pathway activity control DC-orchestrated immune responses. (buyresearchchemicalss.net)
  • Our data reveal that DC differentiation requires not only improved manifestation of RelB but also raised constitutive activity of the non-canonical NF-κB signaling pathway. (buyresearchchemicalss.net)
  • Our findings demonstrated that BMSCs promote remyelination in the spinal cord of HD-exposed rats via TNFα/RelB-Hes1 pathway, providing novel insights for evaluating and further exploring the therapeutical effect of BMSCs on demyelinating neurodegenerative disease. (biomedcentral.com)
  • RELB has been shown to interact with NFKB2, NFKB1, and C22orf25. (wikipedia.org)
  • NFKB1 or NFKB2 is bound to REL, RELA, or RELB to form the NFKB complex. (avivasysbio.com)
  • NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL, RELA, or RELB. (nih.gov)
  • NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. (abcam.com)
  • or RELB (MIM 604758) to form the NFKB complex.The p50 (NFKB1)/p65 (RELA) heterodimer is the most abundant form of NFKB. (bioinf.org)
  • The NF-κB protein RelB controls dendritic cell (DC) maturation and could be targeted therapeutically to manipulate T cell responses in disease. (buyresearchchemicalss.net)
  • Shape 1 A MEF-based kinetic model will not take into account RelB rules in DCs To adjust the model to DCs we 1st measured the manifestation of crucial NF-κB protein in bone tissue marrow-derived DCs (BMDCs) compared to mouse embryonic fibroblasts (MEFs) and bone tissue marrow-derived macrophages (BMDMs). (buyresearchchemicalss.net)
  • In vitro cultured OPCs showed more differentiation after incubation with BMSC-CM. Hes1 expression was found to be significantly increased by HD and decreased by BMSC or BMSC-CM. The change of Hes1 was found, however, independent of Notch1 activation, but dependent on TNFα/RelB signaling. (biomedcentral.com)
  • NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. (hmdb.ca)
  • RelB:p52 activates the expression homeostatic lymphokines, which instruct lymphoid organogenesis and determine the trafficking of naive lymphocytes in the secondary lymphoid organs. (wikipedia.org)
  • In DCs the molecular control mechanisms must provide for constitutive RelB expression to enable rapid and decisive induction of maturation programs following exposure to pathogens or PAMPs but must limit spontaneous maturation of DCs in their absence. (buyresearchchemicalss.net)
  • HD was found to increase TNFα, RelB and Hes1 expression, and BMSCs were found to have the opposite effect. (biomedcentral.com)
  • Addition of recombinant TNFα to OPCs or RelB overexpression similarly caused upregulation of Hes1 expression. (biomedcentral.com)
  • Most intriguingly, a recent study identified that TNF-induced canonical signalling subverts non-canonical RelB:p52 activity in the inflamed lymphoid tissues limiting lymphocyte ingress. (wikipedia.org)
  • it recapitulates well-documented NF-κB control in MEFs20-22 such as for example fast LPS-induced RelA activation and postponed lymphotoxin β-mediated RelB activation (Fig. Cyclo (-RGDfK) 1b). (buyresearchchemicalss.net)