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 was detected early in pregnancy followed

6 RelB is an NF-kappaB family transcription factor activat

7 RelB is processed by CO2 in a manner dependent on a key

8 RelB knockdown disassociated the complex and reversed tr

9 RelB stabilizes itself by directly interacting with p100

10 RelB, a member of the NF-kappaB family, attenuates cigar

11 RelB, which acts as a repressor of TNFalpha transcriptio

12 RelB-p52 also represses BMF translation by regulating mi

13 the noncanonical NF-kappaB pathway, but as a RelB-p50 dimer regulated by canonical IkappaBs, IkappaBa

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

15 here can prevent amplification of the active RelB:p52 dimer in elevated inflammatory conditions to en

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

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

18 s significantly and potently decreased after RelB overexpression.

19 staining the permissive promoter state after RelB knockdown required ATP-dependent nucleosome remodel

20 factor-kappaB so that in the absence of AhR RelB is prematurely degraded, resulting in heightened in

21 of TRAF3 in thymic epithelial cells allowed RelB-dependent development of normal numbers of AIRE-exp

22 the NF-kappaB pathway and implicate altered RelB/p100-dependent signaling in the CO2-dependent regul

23 oth the classical (p65/p50) and alternative (RelB/p52) NF-kappaB activation pathways, estrogen induce

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

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

26 The mutational state of NOTCH1, p-ERK and RelB could serve as potential biomarkers of tipifarnib s

27 nohistochemistry study showed that p-ERK and RelB were associated as potential biomarkers of tipifarn

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 splayed marked decreases in nuclear RelA and RelB and mRNA expression of proinflammatory mediators co

49 The identified sequences recruit RelA and RelB components of the NF-kappaB transcription complex t

50 eletion in MPCs activated NF-kappaB RelA and RelB to promote RANKL expression and enhance bone destru

51 rough nuclear import and binding of RelA and RelB transcription factors to the PLPP3 promoter and sug

52 sociation with increases in nuclear RelA and RelB, components of the classical and alternative NF-kap

53 ory and developmental signaling via RelA and RelB, respectively.

54 dimerization with a limited pool of RelA and RelB.

55 ivated the NF-kappaB family member RelB, and RelB recruited the histone methyltransferases G9a and SE

56 ted NAD(+) levels concomitant with SIRT1 and RelB accumulation at the TNF-alpha promoter of endotoxin

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

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

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

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

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

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

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

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

65 RANKL-induced osteoclastogenesis induced by RelB overexpression.

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

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

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

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

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

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

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

73 experiment, small inhibitory RNAs decreased RelB expression in tolerant cells and restored endotoxin

74 is in sharp contrast to the well documented RelB stabilization and induction by high dose LPS, poten

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

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

77 ar to WT controls, but the absence of either RelB or NIK completely blocked the tumor-induced loss of

78 e received a recombinant adenovirus encoding RelB by intranasal aspiration to induce transient RelB o

79 B promoted DC activation not as the expected RelB-p52 effector of the noncanonical NF-kappaB pathway,

80 ature requires induction of NF-kappaB factor RelB, which directs histone H3K9 dimethylation, disrupts

81 reported that NF-kappaB transcription factor RelB and histone H3 lysine methyltransferase G9a directl

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

83 uction of the NF-kappaB transcription factor RelB by endotoxin activation is necessary and sufficient

84 f low expression of the transcription factor RelB in untreated macrophages, high p52 expression repre

85 noncanonical NF-kappaB transcription factor RelB.

86 g kinase (NIK) and the transcription factors RelB and p52 directly suppressed Il17a expression and IL

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

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

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

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

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

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

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

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

95 Higher RelB subunit expression was demonstrated in estrogen rec

96 oderately higher p65 and p50 but much higher RelB.

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

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

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

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

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

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

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

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

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

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

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

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

109 Hypercapnia-induced RelB processing was sensitive to proteasomal inhibition

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

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

112 Interestingly, RelB expression (cytoplasmic and mRNA) was inversely ass

113 omoters, and its ability to repress them, is RelB-dependent, as shown by experiments using relB(-/-)

114 d the nuclear translocation of the NF-kappaB RelB subunit and activated expression and secretion of i

115 ) as a downstream effector of the NF-kappaB, RelB/Bcl-2/Ras-driven pathway that promotes breast cance

116 Moreover, NF-kappaB2, RelB and Bcl3 expression was associated with overall sur

117 he function of the 'nonclassical' NF-kappaB2-RelB pathway is less clear, although T cells lacking com

118 effect involved activation of the NF-kappaB2-RelB signaling pathway and inhibition of the expression

119 ated the relationship between NF-kappaBeta2, RelB, NIK and Bcl3 expression (mRNA and protein) and the

120 NF-kappaBeta2, RelB, NIK and Bcl3 protein expression levels were assess

121 e development of mTECs, because mice lacking RelB, NIK, or IKKalpha, critical components of this path

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

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

124 which have been previously shown to mediate RelB processing.

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

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

127 elevated CO(2), the NF-kappaB family member RelB was cleaved to a lower molecular weight form and tr

128 OX40 activated the NF-kappaB family member RelB, and RelB recruited the histone methyltransferases

129 , but overexpression of the NF-kappaB member RelB dampened Cox-2 expression in all three fibroblast t

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

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

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

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

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

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

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

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

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

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

140 ion via a process we have termed the de novo RelB synthesis pathway, which protects these cells from

141 Once phosphorylated on serine 472, nuclear RelB dissociates from its interaction with the inhibitor

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

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

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

145 Thus, ERK1-dependent regulation of nuclear RelB is critical for MM survival and explains the NIK-in

146 e late CD69(-)Qa2(+) stage in the absence of RelB-dependent medullary thymic epithelial cells (mTECs)

147 mice was detected by increased abundance of RelB and phospho-IkappaB kinase alpha/beta, an indirect

148 components p100 to p52, and accumulation of RelB.

149 lted from hematopoietic-extrinsic actions of RelB.

150 e, increased expression and/or activation of RelB could be a novel therapeutic strategy against acute

151 kappaB pathway, culminating in activation of RelB, has a key and specific role in the differentiation

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

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

154 h its Daxx binding motif prevents binding of RelB and Daxx, resulting in up-regulation of survival ge

155 folic acid injection, as did DNA binding of RelB and NFkappaB2, detected in nuclei isolated from the

156 o the nucleus in response to CO2 A cohort of RelB protein-protein interactions (e.g. with Raf-1 and I

157 so significantly decreased in the context of RelB overexpression.

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

159 IkappaB control of RelB minimized spontaneous maturation but enabled rapid

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

161 Deletion of RelB in DCs further results in an impaired oral toleranc

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 rticular, cytoplasmic and mRNA expression of RelB was related to 5-year OS (P = 0.014 and P = 0.006,

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

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

172 SIRT1 also promoted de novo expression of RelB.

173 lexes can inhibit the enzymatic formation of RelB:p52.

174 t has remained unclear whether the impact of RelB on cDC development is cell-intrinsic or -extrinsic.

175 Small interfering RNA-mediated inhibition of RelB expression prevented repressive nucleosome repositi

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

177 ne array analysis revealed that knockdown of RelB was associated with upregulation of several actin r

178 ll hairpin RNA (shRNA)-mediated knockdown of RelB, but not other nuclear factor kappaB members, abrog

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

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

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

182 Loss of RelB significantly inhibited spheroid formation, ALDH ex

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

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

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

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

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

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

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

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

191 pathways and lead to opposing regulation of RelB.

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

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

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

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

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

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

198 se results reveal a tumor-supportive role of RelB, implicate the NF-kappaB alternative pathway as a p

199 vity, and loss of p100 alters sensitivity of RelB to CO2 Thus, we provide molecular insight into the

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

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

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

203 nucleosome remodeling and its dependence on RelB.

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

205 expressed in NSCLC (P < 0.001 for all), only RelB mRNA levels were strongly increased in cancerous sp

206 ctions to target DNA methyltransferases onto RelB target sites in the genome provides a rare example

207 h other TNF-responsive genes such as Ccl2 or RelB, which suggested that this effect was not a general

208 alternative NF-kappaB components IKKalpha or RelB have reduced mitochondrial content and function.

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

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

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

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

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

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

215 ighly suggestive of assembly of multiple p50/RelB heterodimers on tandem kappaB sites in solution.

216 reveal optimal assembly of two wild-type p50/RelB heterodimers on tandem HIV kappaB DNA with 2 bp spa

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

218 udy, we show that the IKKalpha-dependent p52/RelB noncanonical pathway is critical to sustain CXCL12/

219 The NF-kB signaling, regulated by IKK1-p52/RelB and IKK2-p65, is activated by various stresses to p

220 that nuclear factor kappaB (NF-kappaB) (p52/RelB) is persistently activated in a subset of BRCA1-def

221 aling pathway mediates activation of the p52/RelB NF-kappaB complex and, thereby, regulates specific

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

223 haracterized by nuclear translocation of p52:RelB heterodimers.

224 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

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 d classical NF-kappaB signaling up-regulates RelB expression that inhibits both basal and NC NF-kappa

230 d with increased binding of p50, p65, c-Rel, RelB, and p300 proteins to a level comparable with that

231 ranscription factors, including RelA, c-Rel, RelB, NF-kappaB1 (p50 and its precursor p105), and NF-ka

232 fied one NF-kappaB, targeted by RelA, c-Rel, RelB, p105/p50, and p100/p52, and two AP-1, targeted by

233 tors consists of five proteins, RelA, c-Rel, RelB, p50, and p52, which assemble into several homodime

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

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

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

237 d inflammatory conditions to ensure reliable RelB-dependent developmental signaling independent of in

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

255 Thus, we provide clear evidence that RelB-dependent pathways regulate the capacity of DCs to

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 hat alternative NF-kappaB activation via the RelB/p52 complex is not solely responsible for Treg accu

288 mp1 represents a novel mechanism whereby the RelB NF-kappaB subunit mediates repression, specifically

289 at DBC1 suppresses B cell activation through RelB inhibition.

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

291 face hydrophobic residues that are unique to RelB does not affect its propensity to form homodimers v

292 by intranasal aspiration to induce transient RelB overexpression in the lungs and were subsequently e

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

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

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

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

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

298 indicate that ARNT functions in concert with RelB in a CD30-induced negative feedback mechanism.

299 by IKKalpha facilitates its interaction with RelB and IKKalpha, indicating that DBC1-mediated suppres

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