ライフサイエンスコーパス: RelA

1 RelA (p65) NF-kappaB, IRF1, and Viperin-dependent IRF7 b

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

3 RelA is recruited to stalled ribosomes and activated to

4 RelA is responsible for (p)ppGpp production during a str

5 RelA was the only synthase that was necessary for vpsT e

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

7 RelA-dependent demethylation occurring upon HBx expressi

8 RelA-P-Ser536 may be a core fibrogenic regulator of fibr

9 RelA/SpoT-homolog proteins synthesize transcriptional mo

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

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

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

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

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

15 iting the interaction of Brd4 and acetylated RelA with the bromodomain extraterminal protein inhibito

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

17 f RelA and the binding of Brd4 to acetylated RelA to facilitate Tax-mediated transcriptional activati

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

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

20 reduced the development of AP in C57BL/6 and RelA-deficient mice.

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

22 6 was associated with senescence bypass, and RelA deficiency in this context attenuated cancer cell p

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

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

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

26 alpha or the combination of IkappaBalpha and RelA selectively were deleted from pancreas of mice usin

27 ncreas-specific deletion of IkappaBalpha and RelA.

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

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

30 -kappaB) (a heterodimer of NF-kappaB1p50 and RelA) is activated rapidly in acute pancreatitis (AP).

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

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

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

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

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

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

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

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

39 ificantly faster than MEFs deficient in both RelA and cRel due to lack of inhibition of BAD by IKK.

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

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

42 on patterns, compared with healthy skin, but RelA distribution was unaltered.

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

44 5 expression in ATDC5 cells was increased by RelA/p65 overexpression and decreased by knockdown throu

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

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

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

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

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

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

51 A phosphorylation event of a well-conserved RelA(Ser276) is prerequisite for the former interaction

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

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

54 forms endogenous complexes with cytoplasmic RelA.

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

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

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

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

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

60 to NF-kappaB-regulated promoters to enhance RelA acetylation.

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

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

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

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

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

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

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

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

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

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

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

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

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 Our results identify RelA as an adaptor with which SCF fine tunes NF-kappaB t

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

77 ation, and histopathology were attenuated in RelA/p65(Deltamye) mice, but not in the absence of STAT-

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

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

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

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

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

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

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

85 iption (STAT) and NF (nuclear factor)-kappaB RelA pathways.

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

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

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

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

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

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

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

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

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

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

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

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

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

99 feedback gene whose expression is NF-kappaB/RelA dependent and requires a functional interaction wit

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

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

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

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

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

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

106 context orchestrate activation of NF-kappaB/RelA sub-pathways differing in biological function and t

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

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

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

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

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

112 Sixteen novel NF-kappaB/RelA-regulated genes and TFBSs were experimentally valid

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

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

115 n of HSCs in vivo, we generated mice lacking RelA/p65 in the hematopoietic compartment.

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

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

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

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

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

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

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

123 tworks and suggested new pathways modulating RelA transcriptional activity.

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

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

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

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

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

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

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

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

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

133 degradation of constitutively active nuclear RelA.

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

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

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

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

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

139 Tax induced the acetylation of lysine 310 of RelA and the binding of Brd4 to acetylated RelA to facil

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

141 The ability of RelA/p65 to directly recruit DNMT-1 to chromatin, result

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

145 Constitutive activation of RelA up-regulates Spi2A, which protects mice against the

146 suppress the tumour-promoting activities of RelA.

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

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

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

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

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

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

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

154 calorimetric analyses allowed the design of RelA-mutants that selectively abrogated the two distinct

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

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

157 two components--first, DNA binding domain of RelA interacts with the KIX domain of CBP/p300, and seco

158 interaction with the Rel homology domain of RelA.

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

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

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

162 The structure reveals the folding of RelA-TA2 (a section of TAD) upon binding to TAZ1 through

163 of the constitutively active nuclear form of RelA.

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

165 Inactivation of RelA accelerated pancreatic lesion formation in Kras mic

166 unctions as a specific targeted inhibitor of RelA-P-Ser536 in vivo and exerts an antifibrogenic effec

167 ssess potential problems with FP labeling of RelA.

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

169 Loss of RelA in the regenerating neuroepithelium perturbs the ho

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

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

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

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

174 psilon) and the transactivating potential of RelA/p65.

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

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

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

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

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

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

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

182 e transcriptional activation domain (TAD) of RelA binds to the TAZ1 domain of CBP/p300.

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

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

185 e latter interaction in the transcription of RelA-activated genes remains unclear.

186 paBalpha results in nuclear translocation of RelA and reduces AP induction and trypsin activation in

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

188 ppaB and subsequent nuclear translocation of RelA.

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

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

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

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

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

194 considered a decisive factor for the overall RelA:CBP/p300 interaction.

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

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

197 We document that the NFkappaB subunit p65 (RelA) interacts with two independent consensus NFkappaB

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

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

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

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

202 which depends on activated IKKalpha and p65/RelA.

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

204 x nuclear translocation did not occur in p65/RelA null murine embryonic fibroblasts.

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

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

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

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

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

210 H9c2 cells revealed sNix suppression of p65/RelA binding to a subset of weaker DNA binding sites, ac

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

218 mitant with nuclear translocation of the p65/RelA subunit of NFkappaB.

219 ix co-localized and co-precipitated with p65/RelA after TNFalpha stimulation; TNFalpha-induced sNix n

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

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 expression of IKKepsilon and phosphorylated RelA was observed in human Kaposi sarcoma.

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

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

232 relieving NF-kappaB suppression by reducing RelA expression.

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

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

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

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

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

238 ivated IKKepsilon promoted NF-kappaB subunit RelA (also known as p65) phosphorylation, which correlat

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

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

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

242 he role of the nuclear factor-kappaB subunit RelA/p65 in the regulation of HSCs in vivo, we generated

243 nslational modifications of the p65 subunit (RelA) are a major aspect of the extremely flexible regul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

260 binding partner of I-kappaB, suggesting that RelA is the linker between USP14 and I-kappaB.

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

262 The RelA:CBP/p300 complex is comprised of two components--fi

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

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

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

266 ence with positively charged residues in the RelA NTD.

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

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

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

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

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

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

273 sion analysis showed that a major set of the RelA-activated genes, larger than previously believed, i

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

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

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

277 abrogated the two distinct components of the RelA:CBP/p300 interaction.

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

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

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

281 Detailed studies of these RelA mutants using cell-based techniques, mathematical m

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

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

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

285 To activate transcription, RelA (a prominent NF-kappaB family member) interacts wit

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

287 th of lung AD cells, at least partially, via RelA-dependent mechanisms.

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

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

290 disruption of NF-kappaB signaling, in which RelA (p65) deletion prevented TNFalpha/IL-1beta inductio

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

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

293 gly, we found that USP14 was associated with RelA, a binding partner of I-kappaB, suggesting that Rel

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

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

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

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

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

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

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