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1 RelB also affected expression of the ALDH gene ALDH1A2 I
2 RelB and RelF act as transcriptional activators, inducin
3 RelB directly increased expression of BECN1, a key autop
4 RelB expression correlated with IL-1beta repression, and
5 RelB expression is relatively higher in untreated KG1a c
6 RelB expression was detected early in pregnancy followed
7 RelB is an NF-kappaB family transcription factor activat
8 RelB is both constitutively present and is inducible by
9 RelB is processed by CO2 in a manner dependent on a key
10 RelB knockdown disassociated the complex and reversed tr
11 RelB stabilizes itself by directly interacting with p100
12 RelB, a member of the NF-kappaB family, attenuates cigar
13 RelB, which acts as a repressor of TNFalpha transcriptio
14 RelB-p52 also represses BMF translation by regulating mi
15 the noncanonical NF-kappaB pathway, but as a RelB-p50 dimer regulated by canonical IkappaBs, IkappaBa
20 staining the permissive promoter state after RelB knockdown required ATP-dependent nucleosome remodel
21 factor-kappaB so that in the absence of AhR RelB is prematurely degraded, resulting in heightened in
22 of TRAF3 in thymic epithelial cells allowed RelB-dependent development of normal numbers of AIRE-exp
23 the NF-kappaB pathway and implicate altered RelB/p100-dependent signaling in the CO2-dependent regul
24 oth the classical (p65/p50) and alternative (RelB/p52) NF-kappaB activation pathways, estrogen induce
26 are inhibitors of NF-kappaB RelA, cRel, and RelB dimers, the atypical IkappaB protein Bcl3 is primar
28 d increases in NF-kappaB-inducing kinase and RelB, which were predominantly located in tubular epithe
29 .g. Lcn2 and A20), as well as IKK1, NIK, and RelB, but no changes in markers of inflammation or fibro
30 or together with LIGHT up-regulated p100 and RelB expression and induced the nuclear localization of
32 NF-kappaB activities, synthesis of p100 and RelB NF-kappaB members, noncanonical NF-kappaB activity,
34 e NF-kappaB2 transcription factors, p100 and RelB, by regulating the NF-kappaB-inducing kinase (NIK).
35 ing pathways, resulting in increased p50 and RelB nuclear translocation and TNFSF15 and OX40L express
36 F-kappaB p100, and nuclear NF-kappaB p52 and RelB, suggesting a BCL10 requirement for activation of t
38 ermore, overexpression of p50, p65, p52, and RelB individually in nfkappab1(-/-) or nfkappab1(+/+) BM
40 f the Cot promoter demonstrated that p65 and RelB bound to the distal NF-kappaB-binding site and that
42 pha activation of both NF-kappaB p50/p65 and RelB/p52 and the increase in intestinal TJ permeability.
47 ed LPC-specific ablation of RelA, c-Rel, and RelB did not phenocopy NEMO deficiency, but constitutive
48 kappaB family proteins (p65, p50, c-Rel, and RelB) with radiolabeled NF-kappaB-binding oligonucleotid
49 splayed marked decreases in nuclear RelA and RelB and mRNA expression of proinflammatory mediators co
50 sociation with increases in nuclear RelA and RelB, components of the classical and alternative NF-kap
52 aB transactivating subunits c-Rel, RelA, and RelB, which seemed functional as judged by induction of
53 ivated the NF-kappaB family member RelB, and RelB recruited the histone methyltransferases G9a and SE
54 ted NAD(+) levels concomitant with SIRT1 and RelB accumulation at the TNF-alpha promoter of endotoxin
56 Kalpha) and IkappaB kinase beta (IKKbeta) as RelB interacting partners whose activation by TNFalpha p
58 otheliosis viral (v-rel) oncogene related B (RelB) subunit is not induced upon TNFalpha treatment in
62 en examined tumor-induced osteolysis in both RelB-/- and NIK-/- mice by using the B16 melanoma model.
64 activated Akt enhanced osteoclastogenesis by RelB-induced Cot, and a dominant-negative form of Akt si
67 pport the role of RelB in OCs, we challenged RelB-/- mice with TNF-alpha in vivo and found a diminish
72 experiment, small inhibitory RNAs decreased RelB expression in tolerant cells and restored endotoxin
73 is in sharp contrast to the well documented RelB stabilization and induction by high dose LPS, poten
76 ar to WT controls, but the absence of either RelB or NIK completely blocked the tumor-induced loss of
77 e received a recombinant adenovirus encoding RelB by intranasal aspiration to induce transient RelB o
78 B promoted DC activation not as the expected RelB-p52 effector of the noncanonical NF-kappaB pathway,
79 ature requires induction of NF-kappaB factor RelB, which directs histone H3K9 dimethylation, disrupts
80 reported that NF-kappaB transcription factor RelB and histone H3 lysine methyltransferase G9a directl
82 uction of the NF-kappaB transcription factor RelB by endotoxin activation is necessary and sufficient
83 f low expression of the transcription factor RelB in untreated macrophages, high p52 expression repre
87 there was no cell-intrinsic requirement for RelB for development of most cDC subsets, except for the
89 ere is an unrecognized but critical role for RelB within the nonhematopoietic niche that controls nor
91 lB chromatin binding was independent of G9a, RelB transcriptional silencing required G9a accumulation
93 P3K14), the NFkappaB DNA binding heterodimer RelB/NFkappaB2, and proteins involved in NFkappaB2 p100
97 These data provide novel insight into how RelB is required to initiate silencing in the phenotype
104 were deficient in ARNT exhibited defects in RelB recruitment to NF-kappaB-responsive promoters, wher
106 esting that p100 processing is a key step in RelB-rescued, RANKL-induced osteoclastogenesis in aly/al
109 Mechanistically, we show that IL-1-induced RelB/p50 complex formation was further promoted by oncos
112 promoter bound and recruited de novo induced RelB, which directed assembly of the mature transcriptio
115 omoters, and its ability to repress them, is RelB-dependent, as shown by experiments using relB(-/-)
116 d the nuclear translocation of the NF-kappaB RelB subunit and activated expression and secretion of i
117 ) as a downstream effector of the NF-kappaB, RelB/Bcl-2/Ras-driven pathway that promotes breast cance
118 he function of the 'nonclassical' NF-kappaB2-RelB pathway is less clear, although T cells lacking com
119 effect involved activation of the NF-kappaB2-RelB signaling pathway and inhibition of the expression
120 e development of mTECs, because mice lacking RelB, NIK, or IKKalpha, critical components of this path
128 elevated CO(2), the NF-kappaB family member RelB was cleaved to a lower molecular weight form and tr
129 OX40 activated the NF-kappaB family member RelB, and RelB recruited the histone methyltransferases
130 , but overexpression of the NF-kappaB member RelB dampened Cox-2 expression in all three fibroblast t
132 tein, activates nuclear factor-kappaB member RelB-mediated survival genes (cIAP1, cIAP2, and cFLIP),
139 specific, as overexpression of RelA, but not RelB, blocked apoptosis and rescued differentiation in R
141 ion via a process we have termed the de novo RelB synthesis pathway, which protects these cells from
142 Once phosphorylated on serine 472, nuclear RelB dissociates from its interaction with the inhibitor
146 Thus, ERK1-dependent regulation of nuclear RelB is critical for MM survival and explains the NIK-in
147 e late CD69(-)Qa2(+) stage in the absence of RelB-dependent medullary thymic epithelial cells (mTECs)
148 mice was detected by increased abundance of RelB and phospho-IkappaB kinase alpha/beta, an indirect
151 e, increased expression and/or activation of RelB could be a novel therapeutic strategy against acute
152 kappaB pathway, culminating in activation of RelB, has a key and specific role in the differentiation
155 h its Daxx binding motif prevents binding of RelB and Daxx, resulting in up-regulation of survival ge
156 folic acid injection, as did DNA binding of RelB and NFkappaB2, detected in nuclei isolated from the
157 o the nucleus in response to CO2 A cohort of RelB protein-protein interactions (e.g. with Raf-1 and I
163 l interfering RNA results in dissociation of RelB from the promoter and partially restores TNF-alpha
164 The transcriptional activation domain of RelB, but not RelA, directly interacts with the processi
166 Moreover, we found that forced expression of RelB in responsive cells induced repressive nucleosome p
168 rst, we find that steady-state expression of RelB is regulated by the canonical pathway and constitut
172 t has remained unclear whether the impact of RelB on cDC development is cell-intrinsic or -extrinsic.
173 Small interfering RNA-mediated inhibition of RelB expression prevented repressive nucleosome repositi
176 ne array analysis revealed that knockdown of RelB was associated with upregulation of several actin r
177 ll hairpin RNA (shRNA)-mediated knockdown of RelB, but not other nuclear factor kappaB members, abrog
179 ecently, high constitutive nuclear levels of RelB have been observed in human prostate cancer specime
186 results indicate that the overexpression of RelB restores RANKL-induced osteoclastogenesis by activa
188 provide new insights into the regulation of RelB activity and reveal a novel link between selective
197 se results reveal a tumor-supportive role of RelB, implicate the NF-kappaB alternative pathway as a p
198 vity, and loss of p100 alters sensitivity of RelB to CO2 Thus, we provide molecular insight into the
200 This association-mediated stabilization of RelB implies a possible role for RelB in the processing
202 ected cells and restores the upregulation of RelB during differentiation by increased transcriptional
205 ctions to target DNA methyltransferases onto RelB target sites in the genome provides a rare example
206 h other TNF-responsive genes such as Ccl2 or RelB, which suggested that this effect was not a general
207 alternative NF-kappaB components IKKalpha or RelB have reduced mitochondrial content and function.
209 kappaB components, including NFkappaB2/p100, RelB, and NIK, accompanied by processing of NFkappaB2/p1
212 sured by nuclear translocation of RelA, p50, RelB, and p52, and this culminated in the transactivatio
214 ighly suggestive of assembly of multiple p50/RelB heterodimers on tandem kappaB sites in solution.
215 reveal optimal assembly of two wild-type p50/RelB heterodimers on tandem HIV kappaB DNA with 2 bp spa
217 udy, we show that the IKKalpha-dependent p52/RelB noncanonical pathway is critical to sustain CXCL12/
218 The NF-kB signaling, regulated by IKK1-p52/RelB and IKK2-p65, is activated by various stresses to p
219 that nuclear factor kappaB (NF-kappaB) (p52/RelB) is persistently activated in a subset of BRCA1-def
220 aling pathway mediates activation of the p52/RelB NF-kappaB complex and, thereby, regulates specific
223 ory form, and reduced nuclear NF-kappaB p65, RelB, p50, and p52, and IKKalpha were observed in KA/KA
225 -10 promoter and preferentially recruits p65/RelB to IL-12 p35 and p40 promoters, causing a decrease
229 In vivo, D(3) analog resulted in reduced RelB in DCs from VDR WT mice but not VDR knockout mice.
230 d classical NF-kappaB signaling up-regulates RelB expression that inhibits both basal and NC NF-kappa
231 d with increased binding of p50, p65, c-Rel, RelB, and p300 proteins to a level comparable with that
232 ranscription factors, including RelA, c-Rel, RelB, NF-kappaB1 (p50 and its precursor p105), and NF-ka
233 fied one NF-kappaB, targeted by RelA, c-Rel, RelB, p105/p50, and p100/p52, and two AP-1, targeted by
234 tors consists of five proteins, RelA, c-Rel, RelB, p50, and p52, which assemble into several homodime
242 lation of NLRP12 promoted NIK stabilization, RelB nuclear translocation, and increased osteoclastogen
243 egulated the expression of NF-kappaB subunit RelB and blocked the anti-IgM-induced decline in c-Myc a
244 ts were caused by impaired NF-kappaB subunit RelB and p50 activation and by impaired caspase 1-mediat
247 a novel function of the NF-kappaB subunits, RelB/p50, as transcriptional activators of the FA/BRCA p
249 ages by removing transcriptional suppressive RelB through interleukin receptor-associated kinase 1 an
250 o the distal NF-kappaB-binding site and that RelB but not p65 bound to the proximal NF-kappaB-binding
251 aken together, our findings demonstrate that RelB can repress proinflammatory gene expression, and su
252 Taken together, these data demonstrate that RelB is a CO(2)-sensitive NF-kappaB family member that m
254 In the present study, we demonstrate that RelB plays an important radioprotective role in aggressi
257 RelB silences gene expression and found that RelB induces facultative heterochromatin formation by di
258 udy, we examined this paradox and found that RelB, another member of the NF-kappaB family, is induced
262 d-type and Relb(-/-) bone marrow showed that RelB exerts cell-extrinsic actions on some lineages, but
263 flammatory gene expression, and suggest that RelB expression in sepsis patient blood leukocytes may p
267 ion, our study shows for the first time that RelB is required for the cisplatin/TNF-alpha-induced cyt
270 ized a new de novo synthesis pathway for the RelB NF-kappaB subunit, induced by the cytomegalovirus I
272 repeat domain of p105 is not involved in the RelB-p105 complex formation, all domains and flexible re
273 actor-kappaB (NF-kappaB) pathway, mainly the RelB-p52 heterodimer, plays important roles in bone meta
274 specifically activated the RelA but not the RelB form of NF-kappaB in a mucosal epithelial tumor cel
275 es buried within the hydrophobic core of the RelB dimerization domain appears to influence the confor
278 g protein that modulated the activity of the RelB subunit of the transcription factor nuclear factor
280 Given the documented role of several of the RelB-regulated genes in diseases, particularly cancer, t
286 d ovarian cancers NFkappaB signaling via the RelB transcription factor supports TIC populations by di
287 mp1 represents a novel mechanism whereby the RelB NF-kappaB subunit mediates repression, specifically
290 face hydrophobic residues that are unique to RelB does not affect its propensity to form homodimers v
291 by intranasal aspiration to induce transient RelB overexpression in the lungs and were subsequently e
293 our complementary approaches to test whether RelB contributes to tumorigenicity of prostate cancer.
295 unique protein-protein contacts explain why RelB prefers p52 as its dimeric partner for transcriptio
297 indicate that ARNT functions in concert with RelB in a CD30-induced negative feedback mechanism.
298 by IKKalpha facilitates its interaction with RelB and IKKalpha, indicating that DBC1-mediated suppres
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