ライフサイエンスコーパス: RelA

1 RelA is activated during amino-acid starvation, when cog

2 RelA is recruited to stalled ribosomes and activated to

3 RelA promoted the growth of cytopathic RNA viruses by ex

4 RelA, a component of nuclear factor-kappaB (NF-kappaB),

5 RelA-dependent demethylation occurring upon HBx expressi

6 RelA/SpoT-homolog proteins synthesize transcriptional mo

7 uired for MSK1 activation of phospho Ser 276 RelA formation to trigger the IRF7-RIG-I amplification l

8 orylation of the RelA subunit at serine 536 (RelA-P-Ser536) is important for hepatic myofibroblast su

9 ummary, our findings suggest that PPM1A is a RelA phosphatase that regulates NF-kappaB activity and t

10 tivation of the stringent response through a RelA/SpoT homologue (RSH) enzyme-dependent increase in t

11 in vivo, we generated a knockin mouse with a RelA T505A mutation.

12 ence with the interaction between acetylated RelA and Brd4 could be a potential therapeutic approach

13 o viral infections, mammalian cells activate RelA/NF-kappaB heterodimers, which induce genes encoding

14 ment requires signal processing by activated RelA/NF-kappaB.

15 We found that CHPV indeed activated RelA and that RelA deficiency abrogated the expression o

16 Tumor necrosis factor-alpha activates RelA, propagating demethylation to nearby CpG sites, sho

17 ntal mouse osteoarthritis model, ADAMTS5 and RelA were co-localized in chondrocytes of degraded artic

18 6 was associated with senescence bypass, and RelA deficiency in this context attenuated cancer cell p

19 at least two mechanisms involving cRel- and RelA-containing NF-kappaB dimers.

20 folding role in IkappaBalpha degradation and RelA Ser 276 phosphorylation.

21 Rather, we show that HERC3 and RelA are part of a multi-protein complex containing the

22 ncreas-specific deletion of IkappaBalpha and RelA.

23 microarray analyses of the IkappaBalpha- and RelA-deficient pancreata.

24 Here, we identified tumor inhibitory and RelA phosphatase activities of the protein phosphatase 2

25 RelA-FP) construct: RelA-YFP, RelA-mEos2 and RelA-Dendra2.

26 o downregulated in c-rel-/- TCL1-Tg mice and RelA Thr505Ala mutant Emu-Myc mice.

27 on promotes the interaction between MIIP and RelA in the nucleus, by which MIIP prevents histone deac

28 lation as well as the acetylation of p53 and RelA-p65.

29 hich is linked to rifampicin resistance, and RelA F(1)(2)(8)Y, which is associated with an active str

30 , mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and d

31 gh the induction of phosphorylated Stat3 and RelA was compromised after IMQ treatment in the knockout

32 ct genetic evidence substantiating antiviral RelA functions.

33 A cell-autonomous RelA activity amplified the yield of Chandipura virus, a

34 Under stressful conditions, bacterial RelA-SpoT Homolog (RSH) enzymes synthesize the alarmone

35 ng the activation of the IkappaB-kinase beta-RelA NF-kappaB pathway.

36 d when the N-terminal domains (NTDs) of both RelA and p50 were present, even though the interface bet

37 target genes were most often linked to both RelA and c-Rel or to RelA alone.

38 ecular dynamics simulations of the DNA-bound RelA:p50 predicted structural changes in RelA caused by

39 evated synthesis of the (p)ppGpp alarmone by RelA lead to full bypass of the D,D-transpeptidase activ

40 5 expression in ATDC5 cells was increased by RelA/p65 overexpression and decreased by knockdown throu

41 d that the small alarmone ppGpp, produced by RelA and SpoT, is important for stabilizing MglA/SspA an

42 PRMT6 is recruited, by RelA, to selective NF-kappaB target promoters upon TNF-a

43 enetically disabling OIS in Kras mice caused RelA to promote tumor proliferation, suggesting a dual r

44 Moreover, ER*-PRMT6 activation causes RelA accumulation in the nucleus.

45 In virus-infected cells, RelA typically induces the expression of IFN-beta, which

46 We report four cryo-EM structures of E. coli RelA bound to the 70S ribosome, in the absence and prese

47 Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth c

48 elA-fluorescent protein (RelA-FP) construct: RelA-YFP, RelA-mEos2 and RelA-Dendra2.

49 e A (PKAc), ribosmal S6 kinase that controls RelA Ser 276 phosphorylation.

50 forms endogenous complexes with cytoplasmic RelA.

51 evented PA-induced IkappaBalpha degradation, RelA nuclear translocation, NO production, and cytokine

52 tion (ChIP) assays demonstrate HBx-dependent RelA occupancy of NF-kappaB half-site, whereas RelA knoc

53 We show that PPM1A directly dephosphorylated RelA at residues S536 and S276 and selectively inhibited

54 ia coli strains, each expressing a different RelA-fluorescent protein (RelA-FP) construct: RelA-YFP,

55 Consistent with these effects, RelA T505A mice exhibit earlier onset of cancer in the N

56 ring hepatocyte-specific deletions of either RelA or STAT3.

57 anosine tetraphosphate (ppGpp) by the enzyme RelA, a signal typically associated with amino acid star

58 in Escherichia coli by two related enzymes, RelA and SpoT.

59 and the 26S proteasome, thereby facilitating RelA protein degradation.

60 proviral function of the pleiotropic factor RelA linked to its prosurvival properties.

61 ated recruitment of the transcription factor RelA and a histone demethylase, JMJD2A.

62 vation of the NF-kappaB transcription factor RelA was enhanced, whereas nuclear translocation of c-Re

63 mongst ROS-activating transcription factors, RelA/p65 induces Gremlin-1 transcription, which antagoni

64 ve tumor-inhibiting activities; however, few RelA phosphatases have been identified.

65 rine residues S536 and S276, is critical for RelA function.

66 ogether, our data suggest a pivotal role for RelA in regulating OIS in preneoplastic lesions and impl

67 or proliferation, suggesting a dual role for RelA signaling in pancreatic carcinogenesis.

68 Further, RelA mediates MPP+-induced suppression of NF-kappaB acti

69 mediated inhibitions, but potently generated RelA:p52/NF-kappaB activity in a positive feedback loop.

70 ion of the VCAM1 promoter resulted in graded RelA/p65 and RNA polymerase II binding that gave rise to

71 However, structural information about how RelA recognizes stalled ribosomes and discriminates agai

72 However, RelA activates a wide spectrum of genes in physiological

73 ctivation are not fully elucidated; however, RelA phosphorylation, particularly at serine residues S5

74 ochemical and genetic experiments identified RelA as a key player downstream of IKKbeta and IKKepsilo

75 state during exponential growth, implicating RelA and (p)ppGpp levels in the regulation of cell chain

76 for antiviral therapeutic regimes.IMPORTANCE RelA/NF-kappaB participates in a wide spectrum of physio

77 und RelA:p50 predicted structural changes in RelA caused by R30 methylation or a mutation that interf

78 rocesses prevented multiplication of CHPV in RelA-deficient cells.

79 Liver injury was observed in RelA-null (hepRelA(Delta/Delta)) mice but not STAT3-null

80 ction of CYP1A1 was significantly reduced in RelA-deficient MEF compared with wild type MEF cells and

81 d with the disease phenotype and resulted in RelA haploinsufficiency.

82 activates Nf-kappaB signaling, resulting in RelA nuclear translocation and enhanced expression of pr

83 In ATM knockdown cells, TNF-induced RelA Ser 276 phosphorylation is significantly decreased.

84 n reinforcing epithelial innate inflammatory RelA/NF-kappaB response to Citrobacter rodentium infecti

85 racts with NF-kappaB subunit RelA to inhibit RelA DNA binding and target gene activation.

86 In turn, NF-kappaB RelA activation was restored upon deletion of the same s

87 TRAF3 deletion in MPCs activated NF-kappaB RelA and RelB to promote RANKL expression and enhance bo

88 dependent on transcription factors NF-kappaB RelA and STAT3, is a hallmark of these pathologies and o

89 and UBQLN1 provide a link between NF-kappaB RelA and the 26S proteasome, thereby facilitating RelA p

90 We find that FOXO3 binds NF-kappaB RelA in the cytosol, impacting both proteins by preventi

91 tein interaction between FOXO3 and NF-kappaB RelA in tumor-associated DCs.

92 or future studies to use the FOXO3-NF-kappaB RelA interaction as a target to enhance tumor-associated

93 sults show for the first time that NF-kappaB RelA is a critical component regulating the expression o

94 We tracked TNF-stimulated NF-kappaB RelA nuclear translocation by live-cell imaging and then

95 g FOXO3 degradation and preventing NF-kappaB RelA nuclear translocation.

96 paB degradation, (b) alkylated the NF-kappaB RelA protein to prevent DNA binding, and (c) promoted Re

97 tead HERC3 indirectly binds to the NF-kappaB RelA subunit after liberation from IkappaBalpha inhibito

98 ovel mechanism involving FOXO3 and NF-kappaB RelA that controls myeloid cell signaling and impacts th

99 proteins, which are inhibitors of NF-kappaB RelA, cRel, and RelB dimers, the atypical IkappaB protei

100 d with constitutive activation of NF-kappaB (RelA) and increased neutrophil recruitment and elastase

101 echanistically, through repressing NF-kappaB/RelA and STAT3, PDLIM2 increases expression of genes inv

102 oter-associated OGG1 then enhanced NF-kappaB/RelA binding to cis-elements and facilitated recruitment

103 G dinucleotide located adjacent to NF-kappaB/RelA half-site.

104 One of the NF-kappaB/RelA modulators we identified is STAT1.

105 Overall, we have identified 562 NF-kappaB/RelA modulators, which are potential drug targets, and c

106 clarified mechanisms of achieving NF-kappaB/RelA multiple functions through modulators.

107 mutated (ATM), in cytokine-induced NF-kappaB/RelA Ser 276 phosphorylation.

108 This NF-kappaB/RelA site is in a CpG island downstream from EpCAM trans

109 ) at characteristic distances from NF-kappaB/RelA TFBSs.

110 Cat dander induces NF-kappaB/RelA to complex with and activate BRD4, resulting in mod

111 babilistic model to infer 8349 (M, NF-kappaB/RelA, TG) triplets and their modes of modulatory action

112 The inferred (STAT1, NF-kappaB/RelA, TG) triplets were validated by LC-selected reactio

113 To discover modulators of NF-kappaB/RelA, we first identified 365 NF-kappaB/RelA-binding pro

114 ppaB/RelA, we first identified 365 NF-kappaB/RelA-binding proteins using liquid chromatography-tandem

115 listic method yields more accurate NF-kappaB/RelA-regulated networks than a traditional, distance-bas

116 osis by nucleolar sequestration of NF-kappaB/RelA.

117 t RSV induces BRD4 to complex with NF-kappaB/RelA.

118 Mice lacking RelA/p65 specifically in myeloid cells showed impaired r

119 timulation synergistically enhanced the late RelA/NF-kappaB response to TLR4 prolonging NF-kappaB tar

120 lon-deficient cells, yet in response to LPS, RelA dimers also were elevated.

121 vents histone deacetylase 6 (HDAC6)-mediated RelA deacetylation, and thus enhances transcriptional ac

122 ession of AhR and induction of CYP1A1 in MEF RelA null cells.

123 rs for these motifs, NF-kappaB family member RelA/p65 most strongly stimulated the promoter activity.

124 We demonstrate that PRMT1 methylates RelA at evolutionary conserved R30, located in the DNA-b

125 tworks and suggested new pathways modulating RelA transcriptional activity.

126 ng-range allosteric changes in the NFkappaB (RelA-p50) heterodimer induced by DNA or IkappaBalpha bin

127 , even though the interface between NFkappaB(RelA/p50) and IkappaBalpha encompasses only the dimeriza

128 main-only constructs or full-length NFkappaB(RelA/p50).

129 parently indicating that binding of NFkappaB(RelA/p50) stretches the ARD of IkappaBalpha.

130 from the crystal structures of the NFkappaB(RelA/p50)-IkappaBalpha complex.

131 were either free or in complex with NFkappaB(RelA/p50), and were interpreted as being consistent with

132 Restoration of NFkappaB/RelA acetylation by IFRD1 shRNA, cetuximab treatment or

133 at hrHPV impairs the acetylation of NFkappaB/RelA K310 in keratinocytes.

134 ions in the NF-kappaB pathway genes, Nfkbia, RelA and Nfkb1.

135 degradation of constitutively active nuclear RelA.

136 R mice displayed marked decreases in nuclear RelA and RelB and mRNA expression of proinflammatory med

137 ce, in association with increases in nuclear RelA and RelB, components of the classical and alternati

138 Here, we have determined that nuclear RelA reinforces OIS to inhibit carcinogenesis in the Kra

139 endent kinase (CDK)4/6, inhibits the nuclear RelA levels and the expression of NF-kappaB target genes

140 tory factor 1 (IRF1) expression by occluding RelA and IRF3 access to the promoter.

141 for phosphorylation of S(536) and S(468) of RelA, respectively.

142 HBC-selective genetic ablation of RelA (p65), the transcriptional activator of the NF-kapp

143 ibition by combined LPC-specific ablation of RelA, c-Rel, and RelB did not phenocopy NEMO deficiency,

144 We found that the compound ablation of RelA, cRel, and p50, required for canonical NF-kappaB tr

145 Hepatotoxicity in the absence of RelA could be reversed by neutralization of tumor necros

146 The absence of RelA resulted in hepatotoxicity across several models of

147 IkappaBalpha had constitutive activation of RelA and a gene expression profile consistent with NF-ka

148 suppress the tumour-promoting activities of RelA.

149 nd thus enhances transcriptional activity of RelA and facilitates tumor metastasis.

150 primarily determined by the net activity of RelA, a bifunctional (p)ppGpp synthetase/hydrolase, and

151 Additionally, chromatin analyses of RelA target gene promoters showed constitutive recruitme

152 ied proteins suggest that the association of RelA and immunophilins could be direct.

153 ure supports a model in which association of RelA with the ribosome suppresses auto-inhibition to act

154 ession through nuclear import and binding of RelA and RelB transcription factors to the PLPP3 promote

155 ic R30 dimethylation inhibits the binding of RelA to DNA and represses NF-kappaB target genes in resp

156 tion of ATG7 markedly reduced the binding of RelA/p65 to DNA in the nucleus.

157 expression and canonical pathway control of RelA-regulated AhR-responsive gene expression.

158 for the asymmetric arginine dimethylation of RelA and unveil a unique mechanism controlling TNFalpha/

159 The TGS (ThrRS, GTPase and SpoT) domain of RelA binds the CCA tail to orient the free 3' hydroxyl g

160 interaction with the Rel homology domain of RelA.

161 The beneficial effects of RelA were mediated by increased expression of CXCL1 and

162 y identified the core responsive elements of RelA/p65 to be -896/-887 and -424/-415 bp with specific

163 ild type MEF cells and ectopic expression of RelA restored the expression of AhR and induction of CYP

164 of the constitutively active nuclear form of RelA.

165 Loss of the tumor-suppressor function of RelA in the early stages of Kras-driven pancreatic neopl

166 Inactivation of RelA accelerated pancreatic lesion formation in Kras mic

167 ssess potential problems with FP labeling of RelA.

168 n pL2.Lgr5.N2IC mice had increased levels of RelA (which encodes the p65 unit of NF-kappaB) compared

169 nal cells, JQ1 reduced the nuclear levels of RelA NF-kappaB.

170 Loss of RelA in the regenerating neuroepithelium perturbs the ho

171 We suggest a 'short hopping time' model of RelA activity during starvation.

172 cts in fibroblasts, circumvented the need of RelA for their propagation.

173 BRMS1 increases Twist1 promoter occupancy of RelA/p65 K310-a key histone modification associated with

174 ating ligands produced different patterns of RelA and c-Rel signaling dynamic features, such as varia

175 mation and with decreased phosphorylation of RelA (NF-kappaB p65), indicating decreased activation of

176 Phosphorylation of RelA S(536) was required for phosphorylation of S(468),

177 possible role of CBP/p300 in recruitment of RelA to its target promoter sites.

178 Remarkably, the regulation of RelA activity by HERC3 is independent of its inherent ub

179 , we demonstrate that targeted repression of RelA by microRNA-7, as well as subsequent increase in th

180 These results indicate the requirement of RelA-dependent inducible hepatoprotection during pneumon

181 blasts, we genetically dissected the role of RelA in CHPV pathogenesis.

182 JCI, Lesina et al. investigated the role of RelA, the p65 partner of p50 that together form the most

183 To characterize the roles of RelA/(p)ppGpp in glucose starvation response in S. suis,

184 nt the cryo-electron microscopy structure of RelA bound to the bacterial ribosome stalled with unchar

185 Our results contradict an earlier study of RelA-Dendra2 diffusion that inferred off-ribosome synthe

186 ve distinct expression profiles from that of RelA-AP1 and are enriched in introns, CpG islands and DN

187 FKBP52 favors the nuclear retention time of RelA, its association to a DNA consensus binding sequenc

188 B) signaling by imaging the translocation of RelA (p65) to the nucleus.

189 tes IkB and impedes nuclear translocation of RelA (p65), thus repressing oncogenic nuclear factor kap

190 n by the absence of nuclear translocation of RelA with a decreased expression of IL-6, IL-12p40, and

191 ppaB and subsequent nuclear translocation of RelA.

192 quired for thrombin-induced translocation of RelA/p65 to the nucleus, and indeed our results showed t

193 observed in BRMS1(KD) cells are dependent on RelA/p65, the transcriptionally active subunit of nuclea

194 Suppression depends on RelA-directed synthesis of (p)ppGpp, a signalling molecu

195 zoonotic Gram-positive bacterium, while only RelA is functional under glucose starvation.

196 appaB kinase pathway or deletion of c-Rel or RelA resulted in loss of Bach2 expression.

197 While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spo

198 KKbeta or canonical NF-kappaB subunits (p50, RelA/p65, and cRel) to demonstrate that the IKKbeta/NF-k

199 e then chose TLR7, transcription factor p65 (RelA), gamma interferon (IFN-gamma), and IFN-gamma-induc

200 PIAS1 is known to bind to p65 (RelA) in the nucleus and blocks its DNA binding, thus fu

201 ha protein expression, but did not alter p65/RelA levels.

202 er phosphorylation levels of ERK-1/2 and p65/RelA (NF-kappaB) and inducible NO synthase expression, s

203 ximal signaling, it impaired NF-ATc1 and p65/RelA nuclear entry and in vivo responses to OVA peptide.

204 nterferon regulatory factor 3 (IRF3) and p65/RelA.

205 LRRC25 enhanced the interaction between p65/RelA and cargo receptor p62, thus facilitating the degra

206 of the transcription factors NF-kappaB (p65/RelA) and AP1 (c-Fos/c-Jun) to the STIM1 promoter.

207 cathelicidin expression involves myeloid p65/RelA and soluble factor from tumor cells.

208 B alpha (IkappaBalphaSR) blocked nuclear p65/RelA expression and inhibited the proliferation of Ba/F3

209 xLDL-loaded Mvarphis, yet the binding of p65/RelA (the prototypic NF-kappaB family member) was reduce

210 ed with the Rel Homology domain (RHD) of p65/RelA and promotes the degradation of p65/RelA.

211 62, thus facilitating the degradation of p65/RelA through autophagy pathway.

212 p65/RelA and promotes the degradation of p65/RelA.

213 clear factor-kappaB (NF-kappaB) pathway (p65/RelA) in endothelial cells, and this response was depend

214 Silencing of the NF-kappaB proteins (p65/RelA or p50/NF-kappaB1) or the p38 MAPK isoform p38alpha

215 otent because it also directly regulates p65/RelA expression.

216 how that BRCA1 and the NF-kappaB subunit p65/RelA associate constitutively, whereas the p50 NF-kappaB

217 y reduced phosphorylation of its subunit p65/RelA by the chemotherapeutic agent adriamycin (ADR), but

218 ion and acetylation of NF-kappaB subunit p65/RelA.

219 e transducer of NF-kappaB signaling pathway, RelA/p65 is regulated under EGFR activation remains to b

220 pression and nuclear accumulation of phospho-RelA/p65, occurred in both an in vitro model of ACM (exp

221 IKKepsilon, which sequentially phosphorylate RelA in a site-specific manner to enable latent infectio

222 Kinases that phosphorylate RelA promote oncogenic behaviors, suggesting that phosph

223 had higher levels of BCL3 and phosphorylated RelA and IkappaBalpha in inflamed vs noninflamed regions

224 he antagonistic functions of different plant RelA SpoT homologs together modulate ppGpp levels to reg

225 appaBdelta) are known to inhibit preexisting RelA:p50 through sequestration, here we report that p100

226 in human hepatic myofibroblasts, P6 prevents RelA-P-Ser536, but does not affect IKK activation of Ika

227 to MIIP interacting with RelA-this prevents RelA deactylation and enhances transcriptional activity,

228 ein to prevent DNA binding, and (c) promoted RelA polyubiquitination and proteasomal degradation.

229 essing a different RelA-fluorescent protein (RelA-FP) construct: RelA-YFP, RelA-mEos2 and RelA-Dendra

230 next generation sequencing) data, published RelA modulators and TGs, and a compendium of gene expres

231 The identified sequences recruit RelA and RelB components of the NF-kappaB transcription

232 (MSK-1) Ser 376 phosphorylation and reduced RelA Ser 276 phosphorylation, whose formation is require

233 relieving NF-kappaB suppression by reducing RelA expression.

234 n conclusion, microRNA-7, by down-regulating RelA, augments Glut3 expression, promotes glycolysis, an

235 rminal domains of the long RSHs such as Rel, RelA, and SpoT.

236 ng a defect in the translocation of released RelA/p65 to the nucleus in these cells.

237 rus associated also with epidemics, required RelA, and Japanese encephalitis virus, which produced re

238 formation of ampicillin persisters required RelA and that loss of clpA, ssrA, or smpB eliminated per

239 Expression of the phosphorylation-resistant RelA S(536)A increased KSHV lytic gene expression and im

240 The boomerang-shaped RelA with a wingspan of more than 100 A wraps around the

241 than 100 A wraps around the A/R (30S A-site/RelA-bound) tRNA.

242 tivity as knockdown of the NF-kappaB subunit RelA suppresses TRIM29 abundance.

243 Lethe interacts with NF-kappaB subunit RelA to inhibit RelA DNA binding and target gene activat

244 tion in RELA, encoding the NF-kappaB subunit RelA, segregated with the disease phenotype and resulted

245 ll dynamics of two major NF-kappaB subunits, RelA and c-Rel, induced by a panel of pathogen-derived s

246 The (p)ppGpp synthase RelA is activated by ribosomes harboring an uncharged tR

247 Here, two (p)ppGpp synthetases RelA and RelQ are identified in Streptococcus suis, an i

248 he stringent response - (p)ppGpp sythetases [RelA and SpoT] and/or DksA - were defective in biofilm d

249 iors, suggesting that phosphatases targeting RelA could have tumor-inhibiting activities; however, fe

250 und that CHPV indeed activated RelA and that RelA deficiency abrogated the expression of IFN-beta in

251 Our investigation clarified that RelA-dependent synthesis of prosurvival factors restrain

252 We conclude that RelA/p65 is a potent transcriptional activator of ADAMTS

253 alidation experiments, it was confirmed that RelA mRNA is a target of miR-7 and is required for cell

254 and sequential ChIP assays demonstrate that RelA in the presence of HBx forms a complex with EZH2, T

255 Further, the results demonstrate that RelA-dependent gene programs are critical for maintainin

256 We demonstrate that RelA-P-Ser536 is a feature of human lung and skin fibrob

257 and p27(Kip1) (p27) Here we demonstrate that RelA/NF-kappaB activation by Kaposi sarcoma herpesvirus

258 model of PDAC, the authors demonstrated that RelA is a mediator of oncogene-induced senescence (OIS)

259 ng glucose starvation, and demonstrated that RelA/(p)ppGpp plays important roles in adaptation to glu

260 nd pharmacological tools, we determined that RelA activation promotes OIS via elevation of the SASP f

261 nd prolonged mouse survival, indicating that RelA enhances tumor progression in established PDAC.

262 We observe that RelA inducibly binds the native IFN regulatory factor 7

263 We observe that RelA-SP1-enriched promoters have distinct expression pro

264 The structure reveals that RelA utilizes a distinct binding site compared to the tr

265 Our study suggested that RelA might also play a proviral role.

266 The RelA NF-kappaB subunit is activated by acetylation of ly

267 at this NF-kappaB motif is recognized by the RelA/p50 heterodimer.

268 We further show how the RelA:CBP/p300 interaction controls the nuclear response

269 S in preneoplastic lesions and implicate the RelA/CXCL1/CXCR2 axis as an essential mechanism of tumor

270 ence with positively charged residues in the RelA NTD.

271 Unlike RelA knockout mice, the RelA T505A mice develop normally but exhibit aberrant he

272 se mechanisms and illustrate the role of the RelA and SpoT enzymes in the biosynthetic pathway underl

273 Phosphorylation of the RelA subunit at serine 536 (RelA-P-Ser536) is important

274 Acetylation of the RelA subunit of NF-kappaB and the subsequent recruitment

275 Acetylation of the RelA subunit of NF-kappaB at lysine-310 regulates the tr

276 Among these, phosphorylation of the RelA(p65) Thr505 residue has been described as an import

277 expression reduces the initial amount of the RelA/p65 NF-kappaB subunit in cells, contributing to the

278 Enzymes of the RelA/SpoT homology (RSH) family synthesize (p)ppGpp by t

279 ion structure of the latter component of the RelA:CBP complex by NMR spectroscopy.

280 his context, we previously reported that the RelA NF-kappaB subunit represses transcription and mRNA

281 We found that the RelA-specific phenotype in LPS-stimulated cells was phys

282 ly, classical NFkappaB signaling through the RelA transcription factor was equally important for tumo

283 Therefore, RelA is generally considered to be an antiviral transcri

284 starvation induces net binding of all three RelA-FP constructs to 70S ribosomes.

285 (p)ppGpp responds to nitrogen levels through RelA-SpoT homolog enzymes, detecting glutamine concentra

286 The transcripts for TLR7, RelA, IFN-gamma, and IP-10 were significantly downregula

287 st often linked to both RelA and c-Rel or to RelA alone.

288 chronic infections and antibiotic tolerance, RelA represents a good target for the development of nov

289 Unlike RelA knockout mice, the RelA T505A mice develop normally

290 inflammatory and developmental signaling via RelA and RelB, respectively.

291 In this case, classical signaling via RelA was essential for proliferating cells, whereas the

292 lA occupancy of NF-kappaB half-site, whereas RelA knockdown suppresses CpG demethylation and EpCAM ex

293 ta are most consistent with a model in which RelA synthesizes (p)ppGpp while bound to the 70S ribosom

294 It is unclear whether synthesis occurs while RelA is bound to the ribosome or free in the cytoplasm.

295 e propose that the interaction of ComGA with RelA prevents the hydrolysis of (p)ppGpp in K-state cell

296 es replication-transcription conflicts, with RelA activation requiring ribosomal pausing.

297 horylation, leading to MIIP interacting with RelA-this prevents RelA deactylation and enhances transc

298 input and IkappaBepsilon's interactions with RelA- and cRel-specific dimers could account for this st

299 We have discovered that ComGA interacts with RelA and that the ComGA-dependent inhibition of rRNA syn

300 We show that PRMT6 directly interacts with RelA, and that its overexpression enhances the transcrip

301 scent protein (RelA-FP) construct: RelA-YFP, RelA-mEos2 and RelA-Dendra2.