ライフサイエンスコーパス: RelB

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

16 itutively phosphorylated in MM and ERK1 is a RelB kinase.

17 Unlike its transcriptional activities, RelB acted independently of both p52 and p50 in the supp

18 Additionally, RelB-/- precursors fail to form OCs in culture, and this

19 s significantly and potently decreased after RelB overexpression.

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

25 ession of the transcription factors PU.1 and RelB.

26 are inhibitors of NF-kappaB RelA, cRel, and RelB dimers, the atypical IkappaB protein Bcl3 is primar

27 ated with induction of nuclear cyclin D1 and RelB/p52 NF-kappaB complexes.

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

31 Enhanced p100 and RelB expression was inhibited by IKKbeta(K44M), which le

32 NF-kappaB activities, synthesis of p100 and RelB NF-kappaB members, noncanonical NF-kappaB activity,

33 NF-kappaB family members p100 and RelB translocate to the nucleus in response to CO2 A coh

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

37 In several respects the RelB-p52 and RelB-p100 complexes are unique in the NF-kappaB family.

38 ermore, overexpression of p50, p65, p52, and RelB individually in nfkappab1(-/-) or nfkappab1(+/+) BM

39 NF-kappaB family members, p65, p50, p52, and RelB, were inhibited by BCL10 silencing.

40 f the Cot promoter demonstrated that p65 and RelB bound to the distal NF-kappaB-binding site and that

41 lected by elevated nuclear levels of p65 and RelB, respectively.

42 pha activation of both NF-kappaB p50/p65 and RelB/p52 and the increase in intestinal TJ permeability.

43 the activation of both NF-kappaB p50/p65 and RelB/p52 pathways.

44 Chromosomally encoded ParD and RelB proteins function as antitoxins, inhibiting their a

45 In contrast, c-Rel and RelB had little effect on promoter activity.

46 Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but

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

51 dimerization with a limited pool of RelA and RelB.

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

55 ring sterile inflammation via both STAT3 and RelB/p50 complexes.

56 Kalpha) and IkappaB kinase beta (IKKbeta) as RelB interacting partners whose activation by TNFalpha p

57 for ocular inflammation and disease, such as RelB overexpression.

58 otheliosis viral (v-rel) oncogene related B (RelB) subunit is not induced upon TNFalpha treatment in

59 gene transcripts, including Bcl2L1, Bcl2A1, RelB, Birc3, and Bcl3.

60 The association between RelB and AhR may represent a new therapeutic and more se

61 Binding between RelB and G9a was confirmed by glutathione S-transferase

62 en examined tumor-induced osteolysis in both RelB-/- and NIK-/- mice by using the B16 melanoma model.

63 RANKL-induced osteoclastogenesis induced by RelB overexpression.

64 activated Akt enhanced osteoclastogenesis by RelB-induced Cot, and a dominant-negative form of Akt si

65 processing of p100 and osteoclastogenesis by RelB-induced Cot.

66 saka thyroid), an MAP3K, was up-regulated by RelB overexpression.

67 pport the role of RelB in OCs, we challenged RelB-/- mice with TNF-alpha in vivo and found a diminish

68 Malt1-/- Th cells failed to cleave RelB, a suppressor of canonical NF-kappaB, and exhibited

69 Conversely, RelB upregulation was inhibited in primary human monocyt

70 Conversely, RelB-deficient CD4(+) T cells showed enhanced IL-17 indu

71 eration of two interfacial residues converts RelB to a side-by-side homodimer.

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

74 2) During RelB-dependent endotoxin tolerance, the two nucleosomes

75 In contrast, ectopic RelB expression recapitulated the effects of TNF on NC s

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

81 a pathway dependent on transcription factor RelB and immediate early response 3 (IER3).

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

84 noncanonical NF-kappaB transcription factor RelB.

85 e NF-kappaB family of transcription factors, RelB and cRel.

86 ermined the x-ray crystal structures of five RelB dimers.

87 there was no cell-intrinsic requirement for RelB for development of most cDC subsets, except for the

88 lization of RelB implies a possible role for RelB in the processing of p100 into p52.

89 ere is an unrecognized but critical role for RelB within the nonhematopoietic niche that controls nor

90 Furthermore, RelB and p65 were both independently recruited to the GM

91 lB chromatin binding was independent of G9a, RelB transcriptional silencing required G9a accumulation

92 Here we show that an HDAC4-RelB-p52 complex maintains repressive chromatin around p

93 P3K14), the NFkappaB DNA binding heterodimer RelB/NFkappaB2, and proteins involved in NFkappaB2 p100

94 Higher RelB subunit expression was demonstrated in estrogen rec

95 oderately higher p65 and p50 but much higher RelB.

96 Here, we examined how RelB silences gene expression and found that RelB induce

97 These data provide novel insight into how RelB is required to initiate silencing in the phenotype

98 However, RelB forms complexes with its partners using different i

99 ong activation of the anti-inflammatory IKK1-RelB alternative NF-kB pathway as well as the Lxr.

100 e induction of alternative members IKKalpha, RelB, and p52 occurs late in myogenesis.

101 Regulation of PGC-1beta by IKKalpha/RelB also is mammalian target of rapamycin (mTOR) depend

102 Importantly, RelB is constitutively phosphorylated in MM and ERK1 is

103 ased by diabetes, with the largest change in RelB and p50 (approximately twofold decrease).

104 were deficient in ARNT exhibited defects in RelB recruitment to NF-kappaB-responsive promoters, wher

105 e alternative NF-kappaB signaling pathway in RelB/p52 induction.

106 esting that p100 processing is a key step in RelB-rescued, RANKL-induced osteoclastogenesis in aly/al

107 z(a)anthracene treatment displayed increased RelB/p52 activity.

108 ession, and sepsis patients showed increased RelB when compared with normal controls.

109 Mechanistically, we show that IL-1-induced RelB/p50 complex formation was further promoted by oncos

110 TNF-alpha-induced RelB expression and lentiviral small hairpin RNA (shRNA)

111 Hypercapnia-induced RelB processing was sensitive to proteasomal inhibition

112 promoter bound and recruited de novo induced RelB, which directed assembly of the mature transcriptio

113 Inhibiting RelB in aggressive androgen-independent PC-3 cells by st

114 Daxx interacts with RelB and inhibits RelB-mediated transcriptional activation of the human cI

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

121 hat we engineered accordingly showed DC-like RelB control.

122 Despite the biochemical evidence, LT-, RelB-, p52-deficient mice show discrepant phenotypes.

123 g cascade based on lymphotoxin-beta (LTbeta)/RelB.

124 atory COX-2 and PG production by maintaining RelB expression.

125 which have been previously shown to mediate RelB processing.

126 The NF-kappaB family member RelB has many properties not shared by other family memb

127 d with a loss of the NF-kappaB family member RelB in AhR(-/-) fibroblasts.

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

131 the activity of nuclear factor-kappaB member RelB, among other transcription factors.

132 tein, activates nuclear factor-kappaB member RelB-mediated survival genes (cIAP1, cIAP2, and cFLIP),

133 interacts with alternative NF-kappaB members RelB and p52 through its leucine zipper domain.

134 al activity of alternative NF-kappaB members RelB and p52 upon CD40 stimulation.

135 Surprisingly, these mutant RelB homodimers remain distinct from canonical side-by-s

136 ls distinctive features not observed for non-RelB complexes.

137 ) precursors to differentiate and normalizes RelB and p65 signaling.

138 erfering RNA-mediated RelA knockdown but not RelB silencing.

139 specific, as overexpression of RelA, but not RelB, blocked apoptosis and rescued differentiation in R

140 Notably, RelB promoted a more invasive phenotype in ERalpha-negat

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

143 Furthermore, elevated nuclear RelB was observed in vivo and correlated with hypercapni

144 ronchiolar fibrosis and decreases in nuclear RelB in lung tissue.

145 paB activation, leading to increased nuclear RelB and p52.

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

149 components p100 to p52, and accumulation of RelB.

150 lted from hematopoietic-extrinsic actions of RelB.

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

153 The autocrine activation of RelB-expressing FAE enterocytes by RANKL/RANK induces th

154 While the NIK-dependent activation of RelB-p52 in MM has been reported, we show that regardles

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

158 so significantly decreased in the context of RelB overexpression.

159 Indeed, synthesis control of RelB is the major determinant of noncanonical NF-kappaB

160 IkappaB control of RelB minimized spontaneous maturation but enabled rapid

161 Canonical pathway control of RelB regulated pathogen-responsive gene expression progr

162 Disruption of RelB-HDAC4 complex by a HDAC4-mimetic polypeptide blocks

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

165 Conversely, stable expression of RelB in androgen-responsive LNCaP tumors increased the c

166 Moreover, we found that forced expression of RelB in responsive cells induced repressive nucleosome p

167 Transient expression of RelB inhibited IL-1beta in endotoxin-responsive cells.

168 rst, we find that steady-state expression of RelB is regulated by the canonical pathway and constitut

169 Moreover, we found that expression of RelB was strongly upregulated during inflammation in viv

170 d this defect is rescued by re-expression of RelB, but not by overexpression of p65.

171 SIRT1 also promoted de novo expression of RelB.

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

174 Inhibition of RelB in breast cancer cells repressed cyclin D1 and c-My

175 Finally, double knockdown of RelB and p100 had a minor effect on senescence induction

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

178 We show that the protein level of RelB is significantly reduced in the absence of p100 and

179 ecently, high constitutive nuclear levels of RelB have been observed in human prostate cancer specime

180 rols and was associated with a rapid loss of RelB only in the KO mice.

181 Loss of RelB significantly inhibited spheroid formation, ALDH ex

182 For example, Lys274 of RelB is removed from the protein-DNA interface whereas t

183 However, the overexpression of RelB fails to rescue RANKL-induced osteoclastogenesis in

184 Furthermore, the overexpression of RelB in aly/aly cells rescues RANKL-induced osteoclastog

185 We hypothesized that overexpression of RelB in the airways of mice would dampen acute smoke-ind

186 results indicate that the overexpression of RelB restores RANKL-induced osteoclastogenesis by activa

187 ursors is also restored by overexpression of RelB, but not p65.

188 provide new insights into the regulation of RelB activity and reveal a novel link between selective

189 Consistently, down-regulation of RelB by small interfering RNA targeting also reduced tum

190 pathways and lead to opposing regulation of RelB.

191 -positive ones, due in part to repression of RelB synthesis by ERalpha signaling.

192 ependent on the Rel homology domain (RHD) of RelB.

193 Here, we reevaluated the role of RelB in cDC and myeloid development using a series of ra

194 lts identify a relatively restricted role of RelB in DC development.

195 val and explains the NIK-independent role of RelB in MM.

196 To further support the role of RelB in OCs, we challenged RelB-/- mice with TNF-alpha i

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

199 e that Daxx controls epigenetic silencing of RelB target genes by DNA methylation.

200 This association-mediated stabilization of RelB implies a possible role for RelB in the processing

201 ignaling, inhibited nuclear translocation of RelB and p50, and decreased Bcl-xL levels.

202 ected cells and restores the upregulation of RelB during differentiation by increased transcriptional

203 nucleosome remodeling and its dependence on RelB.

204 Complementary surfaces on RelB and p50, as revealed by the crystal contacts, are h

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.

208 Ectopic expression of relB or RelB knockdown using small interfering RNA demonstrated

209 kappaB components, including NFkappaB2/p100, RelB, and NIK, accompanied by processing of NFkappaB2/p1

210 and induced the nuclear localization of p100-RelB complexes.

211 The p100/RelB precursor yields p52/RelB producing MAdCAM-1, cytok

212 sured by nuclear translocation of RelA, p50, RelB, and p52, and this culminated in the transactivatio

213 the X-ray crystal structure of NF-kappaB p50/RelB heterodimer bound to a kappaB DNA.

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

216 ent IkappaB kinase-alpha activation, and p52/RelB nuclear translocation.

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

221 The p100/RelB precursor yields p52/RelB producing MAdCAM-1, cytokines, and chemokines impor

222 haracterized by nuclear translocation of p52:RelB heterodimers.

223 ory form, and reduced nuclear NF-kappaB p65, RelB, p50, and p52, and IKKalpha were observed in KA/KA

224 und transcriptionally inactive NF-kappaB p65/RelB heterodimers.

225 -10 promoter and preferentially recruits p65/RelB to IL-12 p35 and p40 promoters, causing a decrease

226 Phospho-RelB remains largely nuclear and is essential for Bim re

227 rtners whose activation by TNFalpha promotes RelB phosphorylation at serine 472.

228 The NF-kappaB protein RelB controls dendritic cell (DC) maturation and may be

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

235 selectin expression, and expression of RelA, RelB, and NF-kappaB2 in their spleens.

236 (listed as toxin/antitoxin: MazF/MazE, RelE/RelB, ChpB, YoeB/YefM, and YafQ/DinJ).

237 ond, the noncanonical pathway, that releases RelB from the 100-kDa NF-kappaB2 complex.

238 The mechanism by which Daxx represses RelB target genes remains elusive.

239 ncing and promotes assembly of the repressor RelB.

240 p100 retains RelB in the cytoplasm and inhibits RANKL-induced osteocl

241 Specifically, RelB is shown for the first time to induce expression of

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

245 sed phosphorylation of the NF-kappaB subunit RelB.

246 t of NF-kappaB and instead required subunits RelB and p50.

247 a novel function of the NF-kappaB subunits, RelB/p50, as transcriptional activators of the FA/BRCA p

248 troviral overexpression of NLRP12 suppressed RelB nuclear translocation and OC formation.

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

253 Here, we demonstrate that RelB plays a critical role in promoting fibroblast migra

254 In the present study, we demonstrate that RelB plays an important radioprotective role in aggressi

255 We also provide evidence that RelB and RelE interact directly, both in vitro and in vi

256 We find that RelB forms canonical side-by-side heterodimers with p50

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

259 We report here that RelB reciprocally inhibits ERalpha synthesis in breast c

260 Here we report that RelB promoted DC activation not as the expected RelB-p52

261 Further, we show that RelB serine 472 phosphorylation status controls MMP3 exp

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

264 We suggest that RelB has evolved into a specialized NF-kappaB subunit wi

265 Early analysis suggested that RelB is required for classical dendritic cell (cDC) deve

266 This mode of binding suggests that RelB may allow the recognition of more diverse kappaB se

267 ion, our study shows for the first time that RelB is required for the cisplatin/TNF-alpha-induced cyt

268 The RelB subunit, for example, does not appear as a homodime

269 As the RelB/Blimp-1 pathway similarly required Ras signaling ac

270 ized a new de novo synthesis pathway for the RelB NF-kappaB subunit, induced by the cytomegalovirus I

271 e regions of each protein are engaged in the RelB-p100 complex.

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

276 n part via transcriptional activation of the RelB NF-kappaB subunit.

277 not by a mutant heterodimer where one of the RelB packing surface is altered.

278 g protein that modulated the activity of the RelB subunit of the transcription factor nuclear factor

279 Loss of the RelB transactivation domain alters NF-kappaB-dependent t

280 Given the documented role of several of the RelB-regulated genes in diseases, particularly cancer, t

281 Daxx) is a transcription co-repressor of the RelB-responsive gene promoters.

282 tissues via the canonical activation of the RelB/p50 complexes.

283 Daxx potently represses the RelB target genes dapk1, dapk3, c-flip, and birc3 (ciap2

284 In several respects the RelB-p52 and RelB-p100 complexes are unique in the NF-ka

285 We previously reported that the RelB homodimer could be forced to assemble through domai

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

288 at DBC1 suppresses B cell activation through RelB inhibition.

289 ortezomib-resistant MM cells are addicted to RelB-p52 for survival.

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

292 We also observed that whereas RelB chromatin binding was independent of G9a, RelB tran

293 our complementary approaches to test whether RelB contributes to tumorigenicity of prostate cancer.

294 dicating a potential mechanism through which RelB can regulate inflammatory cell migration.

295 unique protein-protein contacts explain why RelB prefers p52 as its dimeric partner for transcriptio

296 Daxx also forms complexes with RelB while bound to its target sites in the cIAP2 promot

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

299 Daxx interacts with RelB and inhibits RelB-mediated transcriptional activati

300 N-terminal domain of p100/p52 interacts with RelB but not RelA.