ライフサイエンスコーパス: Egr-1

1 Egr-1 (early growth response gene-1) is an immediate ear

2 Egr-1 and Sp1 binding site inactivation or Egr-1 and Sp1

3 Egr-1 bound to the GC-rich SPUR activation element in th

4 Egr-1 exhibited marked induction in livers of SHP-/- mic

5 Egr-1 increased the transcription of HB-EGF (epidermal g

6 Egr-1 is a master transcription factor mediating the exp

7 Egr-1 is a potential therapeutic target for AD.

8 Egr-1 is an inducible transcription factor that recogniz

9 Egr-1 mRNA and protein were transiently induced by HNF4a

10 Egr-1 null mice were protected from diet-induced obesity

11 Egr-1 promoter was activated by E2F1, and the activation

12 Egr-1 regulates tau phosphorylation and Abeta synthesis

13 Egr-1 silencing also reduces levels of beta-secretase 1

14 Egr-1 silencing does not affect levels of cyclin-depende

15 Egr-1 was up-regulated by IGFBP-5 in a MAPK-dependent ma

16 Egr-1, Egr-2, Vitamin D Receptor, MafB/c: Fos and PU.1:i

17 xpression of early growth response factor 1 (Egr-1), a master transcription factor that regulates the

18 ivity of the early growth response factor 1 (Egr-1).

19 ctivation of early growth response factor 1 (Egr-1).

20 ption factor early growth response factor 1 (Egr-1).

21 ction of the early growth response factor-1 (Egr-1) DNA-binding protein.

22 ulation of the early growth response gene-1 (Egr-1), an apparent negative transcriptional factor for

23 ne product, early growth response protein 1 (Egr-1), to examine the functional role of these vasopres

24 for genes encoding early growth response 1 (Egr-1) (transcriptional regulator), cyclooxygenase 2 (CO

25 was localized to an early growth response 1 (Egr-1) and Sp1 overlapping binding site.

26 Early growth response 1 (Egr-1) protein is a critical regulator of genes contribu

27 ranscription factor early growth response 1 (Egr-1) regulates various vascular pathologies and is up-

28 ranscription factor early growth response 1 (Egr-1) when compared with the WT.

29 tween activation of early growth response-1 (Egr-1) and atherosclerosis and also has demonstrated tha

30 ranscription factor early growth response-1 (Egr-1) and enhanced induction of genes encoding the Egr-

31 on the induction of early growth response-1 (Egr-1) and phosphorylation of c-Jun--known mediators of

32 that RAGE regulates early growth response-1 (Egr-1) expression in hypoxia-exposed macrophages.

33 Early growth response-1 (Egr-1) is overexpressed in human prostate tumors and con

34 ranscription factor early growth response-1 (Egr-1) mediates the stimulation of collagen transcriptio

35 in turn, regulates early growth response-1 (Egr-1), a transcription factor of mPGES-1.

36 ess including Elk1, early growth response-1 (Egr-1), and CREB.

37 ade involving E2F1, early growth response-1 (Egr-1), nuclear receptor small heterodimer partner (SHP,

38 omplexes identified early growth response-1 (Egr-1).

39 for the transcription factors ATF-2, Ets-1, Egr-1 and SP1/SP3.

40 of ASMCs(Des-/-) hypertrophy by the Erk-1/2/Egr-1/miR-26a/GSK-3beta pathway is consistent in human r

41 f the five selected genes-CD25 (IL-2Ralpha), Egr-1, Fosl-1, SOCS3, and Irf-4-was confirmed at the pro

42 Aberrant Egr-1 expression is implicated in carcinogenesis, inflam

43 n of HNF4alpha using siRNA largely abrogated Egr-1 promoter activation.

44 Interestingly, E2F1 activated Egr-1 expression in a biphasic fashion as described in b

45 y we use a second marker for brain activity, Egr-1, and evaluate multiple brain regions.

46 In cells containing altered p53 activity, Egr-1 expression was abolished by pharmacological inhibi

47 BD proteins can block them and thereby allow Egr-1 to avoid sequestration in non-functional locations

48 reover, IGFBP-5 induced cell migration in an Egr-1-dependent manner.

49 immediate early genes (IEGs) Arc/Arg3.1 and Egr-1 in the lateral amygdala (LA) and impairs the 'cons

50 expression of transcription factors Sp-1 and Egr-1.

51 e in the gene encoding p204 bound Egr-1, and Egr-1 activated p204 expression.

52 xtracellular signal-regulated kinase 1/2 and Egr-1 appears to be involved in the increased expression

53 on and transcription repression of Bcl-2 and Egr-1, which are downstream targets of ATF5 in C6 and U8

54 ctor (BDNF), a known inducer of DARPP-32 and Egr-1 expression, enhanced Egr-1 binding to H10 in vitro

55 xhibit significantly less ERK activation and Egr-1 expression in both bone marrow and testis in respo

56 ROS level, downregulated JNK activation, and Egr-1 expression in H9c2 cells after H/R.

57 e H/R-induced ROS level, JNK activation, and Egr-1 expression in H9c2 cells in a dose-dependent manne

58 and Sp1 mRNA and nuclear protein content and Egr-1 and Sp1 protein-DNA binding complex formation.

59 cell development, including Pax-5, E2A, and Egr-1, are reduced, while Id1 and Id2 are increased in F

60 Egr-1 by TGF-beta in normal fibroblasts, and Egr-1 was required for stimulation of collagen by Bcr-Ab

61 sion of immediate early genes like c-fos and Egr-1 by the disease mutants.

62 mory-related immediate early genes c-Fos and Egr-1 were normalized or upregulated in hippocampal CA1

63 Both HNF4alpha and Egr-1 expression were dramatically increased in SHP(-/-)

64 ion of mitogen-activated protein kinases and Egr-1 pathways, culminating ultimately into increased ex

65 crease in PKCepsilon promoter methylation at Egr-1 and Sp-1 binding sites, leading to PKCepsilon gene

66 The interaction between Egr-1 and H10 was confirmed in vitro and in vivo by supe

67 on may involve competitive interplay between Egr-1, YB-1, and Smads.

68 Blocking Cdk5 action blocks Egr-1-induced tau phosphorylation but has no effect on B

69 knockdown of BACE-1 almost completely blocks Egr-1-induced amyloidogenic APP processing and Abeta syn

70 ing BACE-1 action, on the other hand, blocks Egr-1-induced amyloidogenic APP processing but does not

71 ow that ERK1/2 activity is required for both Egr-1 and CREB DNA binding to their cognate sequences id

72 Moreover, both Egr-1 mRNA and protein were elevated in explanted sclero

73 t a sequence in the gene encoding p204 bound Egr-1, and Egr-1 activated p204 expression.

74 LPA-induced gene regulation as evidenced by Egr-1 expression.

75 We demonstrate that in COS-7 cells, Egr-1 binds to the BACE-1 promoter and activates BACE-1

76 AMP-response element-binding protein (CREB), Egr-1, and Sp1 transcription factors and that CREB-bindi

77 hows that in prostate cell lines in culture, Egr-1 overexpression correlated with an alteration of p5

78 nase (MAPK) are essential for ATF5-dependent Egr-1 activation and cell proliferation and survival.

79 k-1 phosphorylation abrogates ATF5-dependent Egr-1 activation and cell proliferation and survival.

80 r (U0126) pretreatment, and by knocking down Egr-1.

81 d by TGF-beta, which was sufficient to drive Egr-1 transactivation.

82 nversely, knockdown of SHP by siRNA elevated Egr-1 protein.

83 r of DARPP-32 and Egr-1 expression, enhanced Egr-1 binding to H10 in vitro.

84 differentiation via modulation of a Mek1/Erk/Egr-1 regulatory axis may be useful in designing new the

85 Immature B lymphoma cells that express Egr-1 message and protein constitutively are growth inhi

86 suggest that the domain dynamics facilitate Egr-1's intersegment transfer that involves transient br

87 ved the early-immediate transcription factor Egr-1 (early growth response 1), a key regulator of prof

88 of the early-immediate transcription factor Egr-1 in situ without also blocking the activation of Sm

89 f the major inducers of transcription factor Egr-1 in the hippocampus.

90 n (I/R) injury, and the transcription factor Egr-1 is a master switch for various damage pathways dur

91 pede association of the transcription factor Egr-1 with its targets.

92 The inducible transcription factor Egr-1, which recognizes a 9-bp target DNA sequence via t

93 e up-regulation of the transcription factors Egr-1 and c-Fos and the correlated synthesis of key proi

94 -LO expression via the transcription factors Egr-1 and CREB.

95 MT gene activation and transcription factors Egr-1 and Sp1 in adrenal medulla-derived PC12 cells.

96 etrical roles of the zinc finger domains for Egr-1 to scan DNA efficiently in the nucleus.

97 sion, our study revealed control network for Egr-1 expression through a feedback loop between SHP and

98 JNK2 is required for Egr-1 induction.

99 phorylation of CBP at Ser436 is required for Egr-1 to activate Lhb expression and is a requirement fo

100 these studies suggest an important role for Egr-1, which, by repressing FOXC2 expression, promotes e

101 together, these data reveal novel roles for Egr-1 as a negative regulator of both CCl(4)-induced hep

102 decoy oligodeoxyribonucleotides specific for Egr-1 and CREB, we discovered that Egr-1 and CREB are di

103 gnificantly reduced vascular transcripts for Egr-1 and matrix metalloproteinase (MMP)-2 antigen and a

104 e in vitro observations, induction of c-Fos, Egr-1, and BDNF was attenuated in the D1 cortical barrel

105 ction of immediate early genes (IEGs) c-Fos, Egr-1, and Homer 1a in the amygdala and the nucleus accu

106 tivation of ERK and the expression of c-Fos, Egr-1, Arc, and brain-derived neurotrophic factor (BDNF)

107 cular dynamics (MD) simulations for the free Egr-1 and the Egr-1-DNA complex.

108 In fibroblasts from Egr-1 knockout mice, induction of fibronectin by IGFBP-5

109 with nuclear translocation of the early gene Egr-1 In conclusion, specific and strictly ordered epige

110 eport activation of the immediate-early gene Egr-1 in the lateral amygdala (LA), hippocampus (CA1), a

111 lving activation of the immediate early gene Egr-1.

112 The early growth response gene (Egr-1) codes for a zinc finger transcription factor that

113 via EP(4) activated the EGFR --> ERK1/2 --> Egr-1 pathway, leading to increased Id-1 transcription a

114 However, how Egr-1 mediates the NMDAR signal in neurons has remained

115 Together, this study identifies Egr-1 as a transcriptional activator of the Ppp1r1b gene

116 in certain TGF-beta responses, and identify Egr-1 as a target of inhibition by imatinib.

117 antibody specific for PDGF-BB as well as in Egr-1(-/-) mice.

118 in these organs, were markedly attenuated in Egr-1 null mice.

119 ned by the increase of energy expenditure in Egr-1 null mice.

120 ibroblasts was accompanied by an increase in Egr-1 and YB-1 repressor binding, suggesting that the mo

121 ls undergo proliferation with an increase in Egr-1 message.

122 auses a time- and dose-dependent increase in Egr-1 protein and mRNA levels and enhanced transcription

123 pecific predator odour leads to increases in Egr-1 expression in the AON in a subregion specific mann

124 rom primary and secondary lymphoid organs in Egr-1(-/-) mice.

125 duction of the PNMT promoter and the rise in Egr-1, Sp1 and PNMT mRNA and protein.

126 fibrotic response was profoundly worsened in Egr-1-deficient mice.

127 -/-) cells; thus, these genes, which include Egr-1 and Egr-2, represent candidate mediators of positi

128 esence of competitor DNA duplexes, including Egr-1 decoys.

129 and several transcription factors, including Egr-1, AP-1, ATF-2, and NF-kappaB.

130 ted, wild-type Ras was described to increase Egr-1 transcription factor expression.

131 In addition, increased Egr-1 expression was observed in idiopathic PAH lungs.

132 ma in the mouse was accompanied by increased Egr-1 accumulation in lesional fibroblasts.

133 d context conditioning selectively increased Egr-1 in CA1.

134 oprecipitation assay, which showed increased Egr-1 binding to the HIF-1alpha promoter in response to

135 m patients with scleroderma showed increased Egr-1 levels, which were highest in early diffuse diseas

136 te shock training, Pre rats showed increased Egr-1 mRNA in the prelimbic mPFC relative to Alt-Pre rat

137 Common significant increased Egr-1 responses to NT (relative to vehicle) were found i

138 Hypoxia increases Egr-1 and Sp1 mRNA and nuclear protein content and Egr-1

139 wever, only exposure to a juvenile increases Egr-1 expression in AON vasopressin neurons.

140 Indeed, Egr-1 was both sufficient and necessary for p300 regulat

141 ifferent mutants of p53 were shown to induce Egr-1.

142 2 inactivation and decreased IGFBP-3-induced Egr-1 expression block the autocrine and paracrine loops

143 onoxide donor; CORM-2) blocked hemin-induced Egr-1 expression.

144 15(S)-HETE induced Egr-1 expression in a time-dependent manner in human der

145 15(S)-HETE-induced Egr-1 expression requires Src activation.

146 Histamine-induced Egr-1 expression is dependent on the activation of the H

147 t not p38 and JNK, mediate histamine-induced Egr-1 expression.

148 ut not p38 MAPK, is required for LPA-induced Egr-1 expression in smooth muscle cells.

149 lar signaling pathway leading to LPA-induced Egr-1 expression.

150 histone H4 acetylation, and that PMA induced Egr-1 and ATF-2 binding to the ACE promoter, whereas Ets

151 Our findings indicate that IL-13 induces Egr-1 nuclear accumulation and CREB serine phosphorylati

152 Histamine markedly and rapidly induces Egr-1 mRNA and protein expression in primary human aorti

153 The JNK inhibitor SP600125 inhibited Egr-1 overexpression in H9c2 cells caused by H/R.

154 Instead, Egr-1 transcription was driven by the ERK1/2 pathway, as

155 Interestingly, Egr-1 mRNA exhibited diurnal fluctuation, which was sync

156 F2 regulates H/R-induced ROS/JNK/Egr-1 signaling, which might be an important mechanism b

157 ther there is abnormal intracellular ROS/JNK/Egr-1 signaling.

158 g was impaired, and skin fibroblasts lacking Egr-1 showed reduced migration and myofibroblast transdi

159 we show that the hippocampus of mice lacking Egr-1 displays electrophysiology properties and ultrastr

160 or basal regulation of EPO via AT1R-mediated Egr-1 activation by p21Ras-mitogen-activated protein kin

161 E-induced angiogenesis requires Src-mediated Egr-1-dependent rapid induction of FGF-2.

162 In the LA and mPFC, Egr-1 increased to a similar extent in no shock, immedia

163 dy provides a new therapeutic target, namely Egr-1, for attenuation of elevated leukotriene levels in

164 ion of DARPP-32, whereas a dominant-negative Egr-1 blocked DARPP-32 induction by BDNF.

165 tor, and overexpression of dominant-negative Egr-1 blocked EPO promoter activation by Ang II.

166 In hippocampal primary neurons, Egr-1 binds to BACE-1 and p35 promoters, enhances tau ph

167 Notably, Egr-1 levels, similar to IGFBP-5, were increased in vivo

168 in the fibrotic response, delineate a novel Egr-1-dependent intracellular signaling mechanism that u

169 in kinases and reduced the levels of nuclear Egr-1 protein and phosphorylated ATF-2.

170 MAPK signaling and the induction of nuclear Egr-1 that interacts with IGFBP-5 and promotes fibrotic

171 replication is by repressing the ability of Egr-1 (early growth response-1) to bind and activate the

172 Our studies revealed sustained activation of Egr-1 with subsequent induction of its downstream target

173 ed the phosphorylation of ERK, activation of Egr-1, and expression of TNF-alpha in macrophages treate

174 ed blood flow, tissue hypoxia, activation of Egr-1, PTEN; increased caspases; and reduced survivin.

175 LPS to increase the DNA binding activity of Egr-1 and p65.

176 pathway and is dependent on the activity of Egr-1 upon the BAG3 promoter.

177 f the specific complex indicated that all of Egr-1's three zinc fingers are equally involved in bindi

178 The binding of Egr-1 to HIF-1alpha promoter was corroborated by electro

179 cription was mediated by enhanced binding of Egr-1 to the Id-1 promoter.

180 precipitation assays demonstrated binding of Egr-1 to the PDGF-B promoter.

181 ipitation assays demonstrated the binding of Egr-1, but not Egr-3, to the Arc promoter.

182 Blockade of Egr-1 via forced expression of its dominant-negative mut

183 nduced activation of MAPKs and expression of Egr-1 are dependent on PKC activation.

184 g to acetylation and prolonged expression of Egr-1 in hyperglycemic conditions.

185 dence that histamine regulates expression of Egr-1 in mammalian cells and demonstrate a novel role of

186 Expression of Egr-1 in these cells rescued the extracellular matrix-pr

187 mechanism controls LPA-induced expression of Egr-1 in vascular smooth muscle cells.

188 on, acetylation, and prolonged expression of Egr-1 leading to proinflammatory and prothrombotic respo

189 nd JNK and blocked LPA-induced expression of Egr-1 mRNA and protein.

190 activation, and increased the expression of Egr-1 protein in H9c2 cells.

191 Ectopic expression of Egr-1 restored positive selection in SAP-1 null thymocyt

192 lleling the upregulated tissue expression of Egr-1 that accompanies fibrosis.

193 eover, we observed that tissue expression of Egr-1 was elevated in patients with scleroderma, which s

194 orrelated with increased local expression of Egr-1.

195 athway, which led to increased expression of Egr-1.

196 mice expressing a dominant negative form of Egr-1, which lacks the trans activation domain but retai

197 activity was necessary for the induction of Egr-1 by TGF-beta in normal fibroblasts, and Egr-1 was r

198 lular regulatory mechanism: LPA induction of Egr-1 expression is via LPA cognate receptor (LPA recept

199 r-ss showed rapid and transient induction of Egr-1.

200 ation, we have also investigated kinetics of Egr-1's translocation between two nonspecific DNA duplex

201 Knockdown of Egr-1 in rat hippocampal primary neurons blocks NMDAR-in

202 The level of Egr-1/NGFI-A was decreased in Fgf2 KO mice and was reest

203 Unexpectedly, the levels of Egr-1 mRNA and protein were highly up-regulated in Hnf4a

204 The mRNA and protein levels of Egr-1, a transcription factor, were increased by TNF-alp

205 of function or loss of function mutations of Egr-1.

206 Moreover, overexpression of Egr-1 in primary striatal neurons induced the expression

207 Likewise, overexpression of Egr-1 in rat hippocampal primary neurons causes reductio

208 ppocampal primary neurons, overexpression of Egr-1 induces BACE-1 expression, activates BACE-1, promo

209 Furthermore, overexpression of Egr-1 led to increased promoter activities for both HIF-

210 ssion rapidly via Src-mediated production of Egr-1.

211 site and within the gene promoter region of Egr-1 (early growth response protein 1) specifically in

212 IP-2, IL-17A did not affect up-regulation of Egr-1 by TCA, indicating that IL-17A does not affect bil

213 a novel role of PKCdelta in up-regulation of Egr-1 expression.

214 vealed that hypoxia-induced up-regulation of Egr-1 is mediated by RAGE signaling.

215 sential for hypoxia-stimulated regulation of Egr-1, at least in part through protein kinase C betaII,

216 ) betaII is a critical upstream regulator of Egr-1 in response to vascular stress.

217 of EGR-1 and NAB2, the latter a repressor of Egr-1.

218 tly, these results suggest a central role of Egr-1 in histamine-induced gene expression and in histam

219 induced angiogenesis, we studied the role of Egr-1.

220 Herein, we report that silencing of Egr-1 in the hippocampus by shRNA reduces tau phosphoryl

221 mechanism that underlies the stimulation of Egr-1, demonstrate for the first time sustained Egr-1 up

222 erall, a lower sensitivity to NT in terms of Egr-1 reactivity in the maternal state was highlighted a

223 n in 3T3 cells of p204 together with that of Egr-1.

224 involves ERK1/2-mediated transactivation of Egr-1, which in turn increases the secretion of EGFR lig

225 nscription factors, whereas transcription of Egr-1 and Fosl-1 was induced by the MEK-ERK pathway.

226 In particular, the zinc finger 1 (ZF1) of Egr-1 in the nonspecific complex is mainly dissociated f

227 Egr-1 and Sp1 binding site inactivation or Egr-1 and Sp1 siRNA inhibit PNMT promoter stimulation by

228 , did not change the levels of CREB, Sp1, or Egr-1 binding to the Galphas promoter, but it induced a

229 s NDRG1 transcription through an overlapping Egr-1/Sp1 binding site that acts as a major site of posi

230 igenetic mechanism in fibrogenesis and place Egr-1 upstream in TGF-beta-driven stimulation of p300 ge

231 Collectively, these results position Egr-1 downstream of c-Abl in the fibrotic response, deli

232 Our current study of the zinc-finger protein Egr-1 (also known as Zif268) and its nuclease derivative

233 -DNA association for the zinc-finger protein Egr-1.

234 ription via early growth response 1 protein (Egr-1).

235 On the contrary, HNF4alpha siRNA reduced Egr-1 expression at both the mRNA and protein levels, an

236 gnal initiated by RAGE ligand AGEs regulates Egr-1 in a manner requiring mDia-1.

237 ream component of the ERK pathway, regulates Egr-1 expression in HAECs.

238 regulatory mechanism: histamine up-regulates Egr-1 expression in primary HAECs via the H1 receptor an

239 Therefore, H/R activates ROS/Egr-1 signaling pathway in H9c2 cells, and JNK activatio

240 uctal gray, virgin mice showed a significant Egr-1 increase with NT (relative to vehicle), but matern

241 overlapping binding consensus sites for SP1, Egr-1, and AP-2), bases C(-71) and C(-59), and an NFkapp

242 -71) and C(-59); both Cs are part of the SP1/Egr-1-binding sites.

243 st, transgenic mice with fibroblast-specific Egr-1 overexpression showed exuberant tissue repair, wit

244 The ability of TGF-beta to stimulate Egr-1 was preserved in Smad3-null mice and in explanted

245 -1, demonstrate for the first time sustained Egr-1 up-regulation in fibrotic lesions and suggests tha

246 Our data demonstrate that Egr-1 achieves the optimal search at physiological ionic

247 We demonstrate that Egr-1 is a transcription repressor of the PSD-95 gene an

248 The present study demonstrates that Egr-1 mRNA expression has a complex relationship to fear

249 cific for Egr-1 and CREB, we discovered that Egr-1 and CREB are directly involved in regulating 15-LO

250 Finally, we found that Egr-1, a protein not associated previously with either I

251 To test the hypothesis that Egr-1 function may be partially compensated by other Egr

252 To test the hypothesis that Egr-1 is important for B cell development, we examined B

253 Therefore, we hypothesized that Egr-1 is required for the development of hepatic fibrosi

254 in immunoprecipitation assay identified that Egr-1, AP-2, and NFkappaB bind to the promoter in HYAL-1

255 tin immunoprecipitation assays indicate that Egr-1 and Sp-1 mediate TSA-induced NAG-1 expression.

256 Our data indicate that Egr-1 is involved in NMDAR-mediated PSD-95 down-regulati

257 Our data indicate that Egr-1 promotes Abeta synthesis via transcriptional activ

258 Our NMR data indicate that Egr-1 undergoes highly dynamic domain motions when scann

259 Here we observed that Egr-1 expression in white adipose tissue (WAT) was highl

260 nal analysis of FGF-2 promoter revealed that Egr-1 binding site proximal to transcription start site

261 e results point to the fundamental role that Egr-1 plays in the regulation of transforming growth fac

262 Here we show that Egr-1 expression is tightly regulated by nuclear recepto

263 Findings suggest that Egr-1 and Sp1 through synergistic interaction are critic

264 tional activation of BACE-1 and suggest that Egr-1 plays role in activation of BACE-1 and acceleratio

265 Our data suggest that Egr-1's kinetic properties are well suited for efficient

266 tivities of Cdk5 and BACE-1, suggesting that Egr-1 is a potential therapeutic candidate for the treat

267 lation in fibrotic lesions and suggests that Egr-1 has a role in the induction and progression of fib

268 tients with scleroderma, which suggests that Egr-1 may be involved in tissue repair and fibrosis.

269 These results showed for the first time that Egr-1 regulates NDRG1 transcription through an overlappi

270 lear factor 4alpha (HNF4alpha) activated the Egr-1 promoter through three DR1 response elements as id

271 sphorylated Elk-1 to the SRE, activating the Egr-1 promoter.

272 Additionally, the Egr-1-mediated induction of HIF-1alpha and FLAP promoter

273 (MD) simulations for the free Egr-1 and the Egr-1-DNA complex.

274 and enhanced induction of genes encoding the Egr-1-regulated proinflammatory chemokines monocyte chem

275 ay in the target association process for the Egr-1 zinc-finger protein is the one involving intersegm

276 Transient transfection of the Egr-1 gene into HeLa cells also resulted in up-regulatio

277 RNA levels and enhanced transcription of the Egr-1 gene via serum response elements in normal fibrobl

278 ARE and serum response element (SRE) of the Egr-1 promoter, which facilitates binding of extracellul

279 he ATF5 response element (ARE) region of the Egr-1 promoter.

280 ing induced the nuclear translocation of the Egr-1 transcription factor, and overexpression of domina

281 e measured the target search kinetics of the Egr-1 zinc-finger protein at various ionic strengths bet

282 pp, we have studied the translocation of the Egr-1 zinc-finger protein in the target DNA association

283 accelerated the target search process of the Egr-1 zinc-finger protein.

284 ation of decoys on the search process of the Egr-1 zinc-finger protein.

285 a activity, as well as its enrichment on the Egr-1 promoter, were markedly repressed by small heterod

286 ion of E2F1, SHP, and EID1 proteins with the Egr-1 promoter, and their direct protein interactions we

287 n profile overlapped only partially with the Egr-1-regulated gene profile.

288 and that activation occurs via TLR2 or TLR4, Egr-1, and MAPK pathways.

289 t mediate ERK and JNK activation, leading to Egr-1 expression, we found that LPA-induced activation o

290 , and c-Jun N-terminal kinase (JNK) prior to Egr-1 induction.

291 ws structural and functional similarities to Egr-1, these two related early-immediate transcription f

292 wild-type p53 was not sufficient to trigger Egr-1 transcription, four different mutants of p53 were

293 n Bim promoter region, while E1A upregulated Egr-1, which was directly involved in Bim transactivatio

294 prove zinc-finger technology, which has used Egr-1 (Zif268) as a major scaffold for engineering.

295 r PlGF-mediated regulation of HIF-1alpha via Egr-1, which results in increased FLAP expression.

296 ein constitutively are growth inhibited when Egr-1 is down-regulated by negative signals from BCR or

297 aspects of the DNA-scanning process in which Egr-1 is nonspecifically bound to DNA and perpetually ch

298 e stimulation, AhR was found in complex with Egr-1 and activator protein-2, which are 2 other nuclear

299 ding protein (CBP) is known to interact with Egr-1, the major mediator of GNRH action on the Lhb gene

300 CBP at Ser436 increased the interaction with Egr-1 on the Lhb promoter, loss of this phosphorylation