ライフサイエンスコーパス: ATF3

1 mma), and activating transcription factor 3 (ATF3).

2 argely dependent on the regulation of p53 by ATF3.

3 with failure to express Il22, Il10, Il9, and Atf3.

4 e promoter of the transcriptional repressor, ATF3.

5 emia/reperfusion by inhibiting expression of ATF3.

6 patic Sort1 and increased VLDL secretion via Atf3.

7 h an additional feedback mechanism involving ATF3.

8 of disruption of the E6-E6AP interaction by ATF3.

9 qPCR confirmed an early upregulation of Atf3.

10 Moreover, up-regulation of ATF3 (a marker of neuronal injury) in vitro could be pre

11 port that activating transcription factor 3 (ATF3), a broad DNA damage sensor whose expression is fre

12 port that activating transcription factor 3 (ATF3), a common stress mediator and a p53 activator, is

13 rate that activating transcription factor 3 (ATF3), a common stress sensor, can activate the tumor su

14 rate that activating transcription factor 3 (ATF3), a hub of the cellular adaptive response network,

15 port that activating transcription factor 3 (ATF3), a member of the ATF/cyclic AMP response element-b

16 ession of activating transcription factor 3 (ATF3), a nuclear calcium-regulated gene and member of th

17 very that activating transcription factor 3 (ATF3), a stress response protein, profoundly affects the

18 port that activating transcription factor 3 (ATF3)-a broad stress sensor-suppressed hormone-induced p

19 here was minimal coexpression of p75NTR with ATF3, a marker for cell stress, but 85% coexpressed the

20 ATF3, a member of the 'enlarged' AP-1 family, is selecti

21 nd the metastatic lung were all dependent on Atf3, a stress-inducible gene, in the noncancer host cel

22 Like CSL, ATF3, a stress-responsive transcriptional repressor, is

23 to gluconeogenic promoters by up-regulating ATF3, a transcriptional repressor that also binds to cAM

24 We found that ATF3 acted as a transcriptional repressor and regulated

25 Moreover, the ER stress target Atf3 acted at the SORT1 promoter region as a transcripti

26 Whereas we demonstrated that ATF3 activated p53 and promoted its pro-apoptotic activi

27 a microarray analysis in quadriceps revealed ATF3 affects genes modulating chemotaxis and chemokine/c

28 Interestingly, loss of Atf3 also promoted spontaneous tumorigenesis in Trp53(+/

29 Activating transcription factor 3 (ATF3), an NMD target and a key stress-inducible transcri

30 We show that ATF3 and ATF4 form a complex capable of binding to the N

31 itiation factor 2alpha, and the induction of ATF3 and ATF4.

32 in the absence of Atf4 also occurred for the Atf3 and C/EBP homology protein (Chop) genes, but not fo

33 nctional tumor suppressor targets, including Atf3 and Cbx7.

34 rotein (CHOP), and reveal that BAP1 binds to ATF3 and CHOP promoters and inhibits their transcription

35 In cardiomyocytes, Atf3 and Egr1 mRNAs are upregulated via ERK1/2 signallin

36 jury are characterized by an upregulation of Atf3 and extensive downregulation in genes associated wi

37 ckle (BK-SS) mice showed increased levels of ATF3 and increased expression of ET-1.

38 NA-494 significantly attenuated the level of ATF3 and induced inflammatory mediators, such as IL-6, m

39 RING finger can bind to the Basic region of ATF3 and mediate the addition of ubiquitin moieties to t

40 downstream of RNA polymerase II peaks at the ATF3 and other stress responsive genes.

41 MDM2) is a bona fide E3 ubiquitin ligase for ATF3 and regulates ATF3 expression by promoting its degr

42 he up-regulation of BNIP3, BNIP3L, PDCD4 and ATF3 and the activation of caspase-3.

43 Notably, ATF3(-/-) and ATF3-sufficient TIAM2 knockdown neutrophil

44 h through activating transcription factor 3 (ATF3) and C/EBP homologous protein (CHOP), and reveal th

45 3'UTR of activating transcription factor 3 (ATF3) and decreases its transcription.

46 s for the activating transcription factor-3 (Atf3) and mitochondrial uncoupling protein-2 (Ucp2) are

47 e (ChAT), activating transcription factor 3 (ATF3), and cleaved caspase-3.

48 rostate health, and provide a novel role for ATF3, and associated proteins within a large signaling n

49 ers activating transcription factor (ATF) 2, ATF3, and ATF7.

50 F3 using immunoblot-EMSA and confirmed ATF4, ATF3, and CCAAT/enhancer-binding protein beta binding at

51 ChIP analysis of the Jmjd3, Atf3, and Chop genes in Atf4 knock-out cells documented

52 scriptional level via Sirt1/Foxo1/Pgc1alpha, Atf3, and Klf15 gene networks.

53 this assay with three protein targets: Akt2, ATF3, and NAEbeta (the beta-subunit of the neddylation a

54 mic reticulum stress response inducing ATF4, ATF3, and NOXA, which can then bind to and inhibit MCL1.

55 NK pathway and its downstream targets, cJUN, ATF3, and the cyclin-dependent kinase inhibitors CDKN1A

56 on using short hairpin RNA (shRNA) amplified ATF3- and NF-kappaB-dependent signaling.

57 Moreover, ATF3 appeared to suppress R175H- and R273H-mediated canc

58 The leucine zipper domain of ATF3 appears indispensable for these effects as an ATF3

59 The ATF3-AR interaction requires the leucine zipper domain o

60 tiple immediate-early (fos, jun, egr1, egr3, atf3, arc, nr4a1) and stress response genes (Ndrg4, Mt1B

61 s such as activating transcription factor 3 (ATF3) are overexpressed.

62 Thus our results reveal a critical role for ATF3 as a key regulator of the acinar cell transcription

63 In conclusion, we identified ATF3 as a regulator in myeloid cells that enhances breas

64 They also identify ATF3 as an important protective factor against endotheli

65 Therefore, we identify NF-kappaB1 and ATF3 as critical mechanisms through which NOD2 downregul

66 e metastasis promoting transcription factor, ATF3, as a downstream target of NDRG1.

67 re we identify the transcriptional regulator ATF3, as an HDL-inducible target gene in macrophages tha

68 Silencing of ATF3, as well as stable introduction of wild-type CSB, r

69 more, we show that association of HDAC6 with ATF3 at its binding site in this promoter was correlated

70 In summary, ATF3 attenuates the expression of inflammation-related g

71 d suppress Atf3 expression, but (as with the Atf3 autorepression loop) inhibition of Egr1 was lost.

72 the latent state, inasmuch as expression of ATF3 bereft of the C-terminal activation domain acts as

73 formed to identify an important role for the ATF3 binding element.

74 RK)-induced activating transcription factor (ATF3) binding to its promoter.

75 CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promote

76 s mutp53-mediated migration, suggesting that ATF3 binds to mutp53 to suppress its oncogenic function.

77 Furthermore, ATF3 bound the proximal MMP13 AP-1 motif in stimulated c

78 port that activating transcription factor 3 (ATF3) bound common mutp53 (e.g. R175H and R273H) and, su

79 As a consequence, ATF3, but not a mutant deficient in MDM2 binding (Delta8

80 trating that negative feedback regulation of Atf3 by Atf3 itself is implausible in this context.

81 Knockdown of neuronal ATF3 by short hairpin RNA abolished the demyelination-in

82 We report here that ATF3 can directly bind the androgen receptor (AR) and co

83 We conclude that ATF3 can suppress mutp53 oncogenic function, thereby con

84 ging evidence suggests that dysregulation of ATF3 contributes to occurrences of human diseases includ

85 However, whether ATF3 contributes to the maintenance of genome stability

86 Even at low basal levels, ATF3 converges with CSL in global chromatin control, bin

87 Thus, ATF3 converges with CSL in negative control of CAF activ

88 Finally, NF-kappaB1 and ATF3 cooperate with other inhibitory pathways, including

89 for multiple DNA binding proteins, including ATF3, CTCF, GABPA, JUND, NANOG, RAD21 and YY1, are enric

90 We identified novel roles for ATF3, CXCL2, DUSP5, JUNB, NEDD9, SELE, TRIB1, and ZFP36

91 ssion of estrogen-responsive genes including ATF3, CYR61 and CTGF, all of which have been implicated

92 Individual silencing of c-Jun, ATF2, or ATF3 decreased cellular survival and revealed c-Jun/ATF2

93 Targeted disruption of ATF3 decreased the effects of ethanol in fasted mice and

94 ession in prostate epithelium, we found that ATF3 deficiency increased cell proliferation and promote

95 tines, the chromosomal instability caused by Atf3 deficiency was largely dependent on the regulation

96 Here we report that Atf3-deficient (Atf3(-/-)) mice developed spontaneous tu

97 Bone marrow-derived MC populations from ATF3-deficient mice are unresponsive to interleukin-3 (I

98 Unexpectedly, ATF3-deficient mice did not exhibit increased airway neu

99 g less efficient breast cancer metastasis in Atf3-deficient mice than in WT mice.

100 enhanced carcinogenic effects of hormones on ATF3-deficient prostates did not appear to be caused by

101 ATF3 deletion was associated with increased lipopolysacc

102 (p38MAPK)-activating transcription factor 3 (ATF3) dependent pathway in A-PECs.

103 on of the immunoregulatory ligand PDL1 in an ATF3-dependent manner and increased the interaction betw

104 and recurrence by promoting metastasis in an ATF3-dependent manner.

105 EGFR- and ATF3-dependent pathways play prominent roles in cancer d

106 Of importance, ATF3-dependent regulation of these genes was observed on

107 PUMA expression is also PERK/ATF3-dependent, through tribbles 3 (TRB3)-regulated AKT

108 s support roles for both cFOS (indirect) and ATF3 (direct) in effecting MMP13 transcription in human

109 ATF3 directly binds Tip60 at a region adjacent to the ca

110 increased lipid body accumulation, and that ATF3 directly regulates transcription of the gene encodi

111 ously developed a mathematical model for the Atf3-Egr1 system.

112 thesis or infection; (ii) in infected cells, ATF3 enhances the accumulation of LAT by acting on the r

113 Conversely, knockdown of ATF3 exacerbates dendritic beading.

114 ent with its role as a potent E6 antagonist, ATF3 expressed enforcedly in HPV-positive SiHa cells act

115 Simultaneous reduction in AK4 and ATF3 expression abolished the inhibitory effects of ATF3

116 clinically occurring tumours, and increased ATF3 expression accounts for suppression of p53-dependen

117 confirmed that elevated cholesterol reduced ATF3 expression and enhanced proliferation of prostate c

118 xonal mitochondria, suggesting that neuronal ATF3 expression and increased mitochondrial transport pr

119 We analyzed the influence of UV radiation on ATF3 expression and its potential role in SCC developmen

120 t negative constructs ameliorated TA-induced ATF3 expression and promoter activities.

121 The current study shows that TA stimulates ATF3 expression and subsequently induces apoptosis.

122 e E3 ubiquitin ligase for ATF3 and regulates ATF3 expression by promoting its degradation.

123 se results, we found that down-regulation of ATF3 expression correlated with lymph node metastasis in

124 suppresses metastasis through inhibition of ATF3 expression followed by activation of the KAI1 gene.

125 sistent DNA damage, which, in turn, controls ATF3 expression in affected cells.

126 ine with these in vivo results, knockdown of ATF3 expression in human prostate cancer cells by single

127 In this study, we demonstrate that ATF3 expression in macrophages is necessary for governin

128 showed a clear trend toward high and nuclear ATF3 expression in nodal DLBCL of the non-GC or ABC subt

129 cogenic stress elicited by Pten loss induced ATF3 expression in prostate epithelium, we found that AT

130 The functional consequences of the loss of ATF3 expression include increased transcription of andro

131 In skeletal muscle, atf3 expression increases after exercise, but its target

132 Induction of ATF3 expression increases transcription throughout the A

133 Although aberrant ATF3 expression is frequently found in human cancers, th

134 including cancer, the mechanism(s) by which ATF3 expression is regulated is largely unknown.

135 Consequently, knockdown of ATF3 expression leads to decreased Tip60 expression and

136 Modulation of ATF3 expression may represent a novel approach to modula

137 ely to play a dominant role in switching off Atf3 expression post-induction.

138 st mutant Htt-N63 toxicity and knocking down ATF3 expression reduced Htt-N63 toxicity in a stable PC1

139 Furthermore, patients with high AK4 and low ATF3 expression showed unfavorable outcomes compared wit

140 UVA induced ATF3 expression through reactive oxygen species-mediated

141 Restoring ATF3 expression under NF-kappaB1 knockdown conditions re

142 Moreover, ATF3 expression was AP-1(cFOS/cJUN)-dependent and expres

143 Consistent with these findings, low ATF3 expression was found to be a poor prognostic marker

144 As a consequence, ATF3 expression was much higher in ABC vs GCB DLBCL cell

145 ffinity for the Atf3 promoter could suppress Atf3 expression, but (as with the Atf3 autorepression lo

146 lly, signals downstream from ERK1/2 suppress Atf3 expression.

147 compared with patients with low AK4 and high ATF3 expression.

148 Knock down of ATF2 abolished TA-induced ATF3 expression.

149 and revealed c-Jun/ATF2-dependent control of ATF3 expression.

150 t increase in c-Jun, c-Fos, c-Myc, Ets2, and ATF3 expressions; and growth factor signaling that proba

151 fewer lung metastases, indicating that host ATF3 facilitates metastasis, at least in part, by its fu

152 extended the model to explore mechanisms of Atf3 feedback regulation.

153 rvation or upregulation of the injury marker ATF3 following prolonged glutamate-gated chloride channe

154 ase II and CSB and the subsequent release of ATF3 from its cAMP response element/ATF target site.

155 elf is a type I IFN-inducible gene, and that ATF3 further modulates the expression of a subset of inf

156 omous program consisting of a stress-induced Atf3-gelsolin cascade affects the change in dendritic sp

157 ssion increases transcription throughout the ATF3 gene locus which requires TFII-I and correlates wit

158 At the ATF3 gene, TFII-I binds immediately downstream of a Pol

159 on of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signal

160 We report here that ATF3 has a central role in MC development and function.

161 Finally, deletion of ATF3 in Apoe(-/-) mice led to in vivo increases in foam

162 Our studies demonstrated that ATF3 in conjunction with HDAC6 acts as a transcriptional

163 results define a previously unknown role for ATF3 in controlling macrophage lipid metabolism and demo

164 ATF3 levels, but results in stabilization of ATF3 in late stages of DNA damage responses.

165 therefore demonstrates an important role for ATF3 in modulating IFN responses in macrophages by contr

166 Here, we reveal that forced expression of ATF3 in motor neurons of transgenic SOD1(G93A) ALS mice

167 nt tumor samples revealed that expression of ATF3 in stromal mononuclear cells, but not cancer epithe

168 Thus, ATF3 in the host cells links a chemotherapeutic agent-a

169 of cancer, and underscore the importance of ATF3 in the maintenance of genome integrity.

170 into account the previously defined role of ATF3 in the SCC development, these findings may provide

171 equently found in human cancers, the role of ATF3 in tumorigenesis is poorly understood.

172 induced inflammation were fully dependent on ATF3 in vitro and in vivo.

173 n induced activating transcription factor 3 (ATF3) in DRG neurons.

174 e role of activating transcription factor 3 (ATF3) in SCC development following treatment with calcin

175 TA treatment and ectopic expression of ATF3 increased apoptosis, whereas knockdown of ATF3 resu

176 , our results of ChIP analysis indicate that ATF3 indeed bound to the promoter of the KAI1 gene.

177 shRNA-mediated block of Atf3 induction suppresses expression of gelsolin, an act

178 stress-associated genes like GRP78, GADD153, ATF3, IRE1alpha, and NOXA in these cells.

179 Thus, ATF3 is a component of a cluster of cellular proteins th

180 ophage lipid metabolism and demonstrate that ATF3 is a key intersection point for lipid metabolic and

181 Our results thus demonstrate that ATF3 is a novel repressor of androgen signaling that can

182 We found that ATF3 is a specifically induced AP1 member in SCC of tran

183 ATF3 to the AKT signaling, and suggest that ATF3 is a tumor suppressor for the major subset of prost

184 Our results thus support that ATF3 is a tumor suppressor in prostate cancer.

185 and demonstrated that genome-wide binding of ATF3 is best explained by considering many dimers in whi

186 by next-generation sequencing, we show that ATF3 is bound to the transcriptional regulatory regions

187 Specifically, (i) ATF3 is induced by stress, such as inhibition of protein

188 the promoter of the LAT precursor RNA; (iii) ATF3 is induced nearly 100-fold in ganglionic organ cult

189 rovide the first evidence demonstrating that ATF3 is regulated by a posttranslational mechanism.

190 Atf3 is required for negative feedback regulation of oth

191 Activating transcription factor 3 (ATF3) is a basic leucine zipper transcription factor tha

192 Activating transcription factor 3 (ATF3) is a common mediator of cellular stress response s

193 Activating transcription factor 3 (ATF3) is a common stress sensor, and its rapid induction

194 Activating transcription factor 3 (ATF3) is a key mediator of the unfolded protein response

195 Activating transcription factor 3 (ATF3) is a member of the ATF/CREB subfamily of the basic

196 Activating transcription factor 3 (ATF3) is an important transcriptional modulator that lim

197 Activating transcription factor 3 (Atf3) is rapidly and transiently upregulated in numerous

198 Additionally, we observed that ATF3 itself is a type I IFN-inducible gene, and that ATF

199 that negative feedback regulation of Atf3 by Atf3 itself is implausible in this context.

200 Tmem119, Olfml3, transcription factors Egr1, Atf3, Jun, Fos, and Mafb, and the upstream regulators Cs

201 genous transcription factor as co-activator (ATF3-JunB) or co-repressor (ATF3-NFkappaB).

202 or transcriptional repression (Stmn2, Ccnd2, Atf3, Klf4, Nodal, and Jun) as well as distinct differen

203 -modulated in skin cancer stromal cells, and Atf3 knockout mice develop aggressive chemically induced

204 ative activity of the prostate epithelium in ATF3 knockout mice that is associated with prostatic hyp

205 Skeletal muscles of ATF3-knockout (ATF3-KO) and control mice were analyzed a

206 ed, we found that hormone-induced lesions in ATF3-knockout mice often contained cells with both basal

207 ligand (cxcl)13 were higher in quadriceps of ATF3-KO mice than in control mice.

208 IIa in quadriceps of control mice but not in ATF3-KO mice.

209 mRNA levels increased after exercise only in ATF3-KO mice.

210 Skeletal muscles of ATF3-knockout (ATF3-KO) and control mice were analyzed at rest, after e

211 ostates (one out of eight mice), the loss of ATF3 led to the appearance of not only PIN but also inva

212 te the addition of ubiquitin moieties to the ATF3 leucine zipper domain.

213 cells, while cholesterol depletion increased ATF3 levels and inhibited proliferation.

214 ncreased HSP60/Cytochrome C (Cyt C) and CHOP-ATF3 levels respectively.

215 on of MDM2 in cells not only increases basal ATF3 levels, but results in stabilization of ATF3 in lat

216 ntiation suggested that acinar cells lacking ATF3 maintain a mature cell phenotype during pancreatiti

217 Dampening the effect of ATF3 may improve the efficacy of chemotherapy.

218 e prediction algorithm suggested that the TF ATF3 may regulate macrophage foam cell formation.

219 er, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhi

220 esent study was performed to observe whether ATF3 mediates TA-induced apoptosis and to elucidate the

221 d died significantly earlier than wild-type (Atf3(+/+)) mice.

222 Here we report that Atf3-deficient (Atf3(-/-)) mice developed spontaneous tumors, and died s

223 y, our promoter-based analysis revealed that ATF3 modulated KAI1 transcription through cooperation wi

224 Consistent with these results, Atf3(-/-) mouse embryonic fibroblasts (MEFs) had more ab

225 nscriptional repressor, whereas knockdown of Atf3 mRNA in ob/ob mice led to increased hepatic sortili

226 NA from the mRNA/miRNA complex, profiles for Atf3 mRNA, Atf3 protein and Egr1 mRNA approximated to th

227 An ATF3 mutant devoid of the mutp53-binding domain failed t

228 ppears indispensable for these effects as an ATF3 mutant lacking this domain failed to interact with

229 ow chimeras revealed a specific reduction in ATF3(-/-) neutrophil recruitment to wild-type lungs.

230 In vitro, ATF3(-/-) neutrophils exhibited a profound chemotaxis de

231 lysis identified ablated Tiam2 expression in ATF3(-/-) neutrophils.

232 as co-activator (ATF3-JunB) or co-repressor (ATF3-NFkappaB).

233 ATF3-null MCs also showed functional defects; high-affin

234 Furthermore, ATF3-null mice lacked MCs in the peritoneum and dermis,

235 els of phosphorylated AKT and S6 proteins in ATF3-null prostate lesions.

236 pression abolished the inhibitory effects of ATF3 on invasion.

237 hose genes and to determine the influence of ATF3 on muscle adaptation to training.

238 immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice.

239 sic transcription, counteract the effects of ATF3 or CSL loss on global gene expression and suppress

240 ATF3 overexpression in AK4-overexpressing cells limits i

241 As a result, Atf3(-/-) pancreatic tissue displayed increased tissue d

242 anslation initiation inhibition and the ATF4/ATF3 pathway, and U bodies rapidly disappeared upon remo

243 These results indicated that ATF3 plays a critical role in toxicity induced by mutant

244 These results indicate that ATF3 plays a key role in a mechanism defending against H

245 -fold in ganglionic organ cultures; and (iv) ATF3 plays a key role in the maintenance of the latent s

246 Importantly, the loss of ATF3 promoted activation of the oncogenic AKT signaling

247 Accordingly, ATF3 promoted the expression of the metastasis suppresso

248 n of the predicted ATF/C/EBP binding site in ATF3 promoter abolished luciferase activation by TA.

249 of ATF2 resulted in significant increase in ATF3 promoter activity, and electrophoretic mobility shi

250 The TA treatment also induced ATF3 promoter activity.

251 on factor (ITF) with a high affinity for the Atf3 promoter could suppress Atf3 expression, but (as wi

252 Activated NRF2 directly binds to ATF3 promoter, thus inducing its expression.

253 Activating transcription factor 3 (ATF3) promotes neuronal survival and axonal growth.

254 Overexpression of ATF3 protects against mutant Htt-N63 toxicity and knocki

255 mRNA/miRNA complex, profiles for Atf3 mRNA, Atf3 protein and Egr1 mRNA approximated to the experimen

256 nthesised miRNAs very efficiently terminated Atf3 protein expression and, with a 4-fold increase in t

257 In turn, ATF3 protein inhibits the expression of various TLR-driv

258 This dual role of ATF3 provides insight into the complex interplay between

259 macrophages from mouse tumors identified an ATF3-regulated gene signature that could distinguish hum

260 In CSB-deficient cells ATF3 remains bound to the promoter, thereby preventing t

261 l death, synaptic activity and expression of ATF3 render hippocampal neurons more resistant to acute

262 ATF3 repressed mutp53-induced NFKB2 expression and sensi

263 Activating transcription factor 3 (ATF3) responds to diverse cellular stresses, and regulat

264 F3 increased apoptosis, whereas knockdown of ATF3 resulted in significant repression of TA-activated

265 known functions in acquired neuroprotection (atf3, serpinb2), memory consolidation (homer1, arc), and

266 nsistent with this, macrophages deficient in Atf3 showed enhanced viral clearance in lymphocytic chor

267 ther, mice with myeloid cell-selective KO of Atf3 showed fewer lung metastases, indicating that host

268 ervation during the course of the disease in ATF3/SOD1(G93A) mice is associated with a substantial de

269 ophagy transcriptional factors such as E2f1, Atf3, Stat1, and Stat3, which may be facilitating myopat

270 Notably, ATF3(-/-) and ATF3-sufficient TIAM2 knockdown neutrophils, both lackin

271 moter contained a consensus binding motif of ATF3, suggesting a possibility that NDRG1 suppresses met

272 As are upregulated via ERK1/2 signalling and Atf3 suppresses Egr1 expression.

273 Here, we demonstrate that ATF3 suppresses the development of prostate cancer induc

274 Although the ATF3 target genes, including dihydrofolate reductase (DH

275 nes, including transcription factors such as ATF3 that are likely to alter the regulation of other ge

276 action requires the leucine zipper domain of ATF3 that independently binds the DNA-binding and ligand

277 crease in activating transcription factor 3 (ATF3), the neuropeptides galanin and neuropeptide Y (NPY

278 Increased Atf3, the most upregulated gene in the RGCL, was confirm

279 Moreover, the ATF3-Tip60 interaction increases the Tip60 stability by

280 Our results thus link ATF3 to the AKT signaling, and suggest that ATF3 is a tu

281 s provide the first genetic evidence linking ATF3 to the suppression of the early development of canc

282 egradation was unlikely caused by binding of ATF3 to the tumor suppressor, but rather was a consequen

283 and to elucidate the molecular mechanism of ATF3 transcription induced by TA.

284 ich was followed by a subsequent increase in ATF3 transcription.

285 Gelsolin, a known target of Atf3 transcriptional activity, is also upregulated.

286 Introduction of an autorepressive loop for Atf3 tuned down its expression and inhibition of Egr1 wa

287 t as well as by other mechanisms, results in ATF3 upregulation, inducing mediators of clinical sympto

288 1 ATF/CRE and ACM sequences to bind ATF4 and ATF3 using immunoblot-EMSA and confirmed ATF4, ATF3, and

289 ring RNA-mediated silencing highlighted that ATF3 was as highly selective for MMP13 as cFOS.

290 Mechanistically, the transcription factor ATF3 was identified as a pivotal regulatory target of AK

291 from these data and the transcription factor ATF3 was identified as a prominent node in the network.

292 Because ATF3 was recently identified as a p53 activator, these r

293 ATF3 was then induced and bound to cytokine gene promote

294 Focusing on ATF3, we observed distinct cognate site preferences conf

295 revealed that hippocampal neurons expressing ATF3 were able to regain their ability for functional sy

296 regulator activating transcription factor 3 (ATF3), which we show by adenovirus driven overexpression

297 ression of activated transcription factor 3 (ATF3), which, in association with accessory proteins (c-

298 es expression of the transcription repressor ATF3, which is necessary and sufficient for suppression

299 It has been reported that ATF3, which may act as an oncogene, is under negative ca

300 bined together, potentiate the expression of ATF3, which may then force SCC development.