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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.
Results suggest that the RelB/NF-kappaB2 pathway regulates T cell migration to autoimmune targets in Sjogren syndrome through TGFbeta (show TGFB1 ELISA Kits)/TGFbetaR-dependent regulation of CXCL12 (show CXCL12 ELISA Kits)/CXCR4 (show CXCR4 ELISA Kits) signaling.
CCR7 (show CCR7 ELISA Kits) overexpression and RelB knockdown (KD) in imDCs improve skin-graft survival in a murine skin-transplantation model. Transfection with Ad-CCR7 (show CCR7 ELISA Kits) and RelB KD in imDCs may be an effective approach inducing immune tolerance, thus being potentially valuable for inhibiting allograft rejection.
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 (show NFKB1 ELISA Kits)-dependent transcriptional activity, and loss of p100 alters sensitivity of RelB to CO2
this study shows that RelB-silencing in dendritic cells generates dendritic cells of tolerogenic properties with immunomodulatory function and appears as potential option of cell-targeted therapy
AhR and NF-kappaB/Rel protein binding profile within the 3'IghRR mediates the inhibitory effects of TCDD on Ig expression and therefore antibody levels.
Relb is necessary for the effective production of downstream RANK(+) medullary thymic epithelial cell progenitors.
we identify in this study a critical role for the combined activity of the RELB and NF-kappaB2 subunits in B cell homeostasis that cannot be compensated for by the canonical NF-kappaB (show NFKB1 ELISA Kits) pathway under physiological conditions.
results indicate that BAFF (show TNFSF13B ELISA Kits) signals coordinate both RelB and cRel activities to ensure survival during peripheral B-cell maturation (show TNFRSF17 ELISA Kits)
phosphorylation of DBC1 at its C terminus by IKKalpha (show CHUK ELISA Kits) facilitates its interaction with RelB and IKKalpha (show CHUK ELISA Kits), indicating that DBC1-mediated suppression of alternative NF-kappaB (show NFKB1 ELISA Kits) is regulated by IKKalpha (show CHUK ELISA Kits).
Low RELB expression is associated with Prostate Cancer.
NF-kappaB (show NFKB1 ELISA Kits) RelB protein, but not RelA (show NFkBP65 ELISA Kits), displayed high expression in Endometrial cancer samples and cell lines.
to elucidate the induced activation of lytic pathway by ionizing radiation, irradiated SNU-719 cells were checked for the RelA (show NFkBP65 ELISA Kits) and RelB expression by real-time PCR. RelB level showed a dose-dependent enhancement on 2nd and 4th day, whereas only a slight upregulation in RelA (show NFkBP65 ELISA Kits) is noticed
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 (show NFKB1 ELISA Kits)-dependent transcriptional activity, and loss of p100 (show CUX1 ELISA Kits) alters sensitivity of RelB to CO2
EZH2 (show EZH2 ELISA Kits), through a methyltransferase-independent mechanism, promotes the transcriptional activation of the non-canonical NF-kappaB (show NFKB1 ELISA Kits) subunit RelB
The altered expression of anti-apoptotic gene Bcl-2 (show BCL2 ELISA Kits) 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
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.
the role of RelB on lymphocyte development in humans was shown.
In conclusion, DECs show a unique hypo-responsive phenotype to the pro-inflammatory stimulus LPS (show IRF6 ELISA Kits) in order to control the inflammatory response at feto-maternal interface.
Bovine foamy virus transactivator BTas interacts with cellular RelB to enhance viral transcription.
XRelB can partially substitute for several, but not all, functions of the Dorsal protein in Drosophila embryos.
NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. 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. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF- kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric RelB-p50 and RelB-p52 complexes are transcriptional activators. Stimulates promoter activity in the presence of p49- and p50-NF-kappa-B. Neither associates with DNA nor with p65-NF-kappa-B (By similarity).
transcription factor RelB
, v-rel avian reticuloendotheliosis viral oncogene homolog B (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3)
, v-rel reticuloendotheliosis viral oncogene homolog B, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3
, avian reticuloendotheliosis viral (v-rel) oncogene related B
, v-rel reticuloendotheliosis viral oncogene homolog B
, transcription factor RelB homolog