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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 d cocaine-induced phospho-ERK activation and Egr-1/Zif268 induction, but without effect on the cocain

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

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

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

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

57 he NAc is required for activation of ERK and Egr-1/Zif268 in D1 dopaminoceptive neurons after acute c

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

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

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

61 i1 directly bound to and repressed c-Fos and Egr-1, as has been shown for Egr-2, all of which are the

62 Erk1/2 and enhanced activation of c-Fos and Egr-1.

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 ated cocaine-induced ERK phosphorylation and Egr-1/Zif268 upregulation in D1-medium spiny neurons and

66 hormone beta subunit gene (Lhb) promoter and Egr-1 as a model system.

67 city, learning, and memory formation such as Egr-1, Arc1, and BDNF specifically in the cerebral corte

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 JNK2 is required for Egr-1 induction.

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

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

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

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

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

106 that Gfi1-mediated downregulation of c-Fos, Egr-1 and Egr-2 may contribute to the role of Gfi1 in gr

107 that Gfi1 inhibits the expression of c-Fos, Egr-1 and Egr-2 through direct transcriptional repressio

108 resulted in diminished expression of c-Fos, Egr-1 and Egr-2, and partially rescued the neutrophil de

109 that Gfi1 inhibited the expression of c-Fos, Egr-1 and Egr-2, and rescued neutrophil development in c

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

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

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

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

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

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

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

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

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

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

120 CS-Rapgef2 expression on cAMP-dependent ERK->Egr-1/Zif268 signaling in cultured neuroendocrine cells;

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 2 inactivation and decreased IGFBP-3-induced Egr-1 expression block the autocrine and paracrine loops

149 15(S)-HETE induced Egr-1 expression in a time-dependent manner in human der

150 15(S)-HETE-induced Egr-1 expression requires Src activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 orrelated with increased local expression of Egr-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 -1, demonstrate for the first time sustained Egr-1 up-regulation in fibrotic lesions and suggests tha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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