ライフサイエンスコーパス: ATF3

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

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

3 e promoter of the transcriptional repressor, ATF3.

4 emia/reperfusion by inhibiting expression of ATF3.

5 patic Sort1 and increased VLDL secretion via Atf3.

6 h an additional feedback mechanism involving ATF3.

7 argely dependent on the regulation of p53 by ATF3.

8 a mechanistic and tumor suppressive role of ATF3.

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

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

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

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

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

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

15 to induce activating transcription factor 3 (ATF3), a repressive transcription factor, which bound to

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

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

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

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

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

21 duced transcriptional reprogramming requires ATF3, a transcription factor that is induced rapidly aft

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

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

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

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

26 ATF3 acts as a suppressor of major proinflammatory gene

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 ATF3 and ATF4 induction downregulated Klotho through alt

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 Egr2, and growth and survival genes such as Atf3 and Gem Based on our results, we propose that early

38 tivating stress-response proteins, including ATF3 and HO-1.

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

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

41 th the well-documented injury-response genes Atf3 and Jun.

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

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

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

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

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

47 3'UTR of activating transcription factor 3 (ATF3) and decreases its transcription.

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

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

50 (DUSP1), activating transcription factor 3 (ATF3), and tribbles pseudokinase 3 (TRIB3), negative reg

51 ATF3 promoter, a synergistic upregulation of ATF3, and a subsequent apoptotic response in cancer cell

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

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

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

55 ain processing, including sprr1a, npy, fgf3, atf3, and cckbr, which were significantly increased.

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

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

58 We observe higher ADORA1, lower ATF3, and lower PD-L1 expression levels in tumor tissues

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

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

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

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

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

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

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

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

67 common signature of GA stress that included ATF3, ARF4, CREB3, and COG6 Taken together, these data i

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

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

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

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

72 upled with gene silencing studies identified ATF3 as the driver of this antitumor synergy.

73 Mechanistically, we identify ATF3 as the factor transcriptionally upregulating PD-L1

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

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

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

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

78 ement for activating transcription factor 3 (ATF3) at -258 to -250 base pairs from the HSF1 transcrip

79 res of ER stress in renal tubular cells with ATF3/ATF4 activation.

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

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

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

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

84 tic mobility shift and ChIP assays confirmed ATF3 binding to this sequence.

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

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

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

88 Transcription factor ATF3 binds to the INS and represses cAMP-dependent promo

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

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

91 activity of HDAC3 is selectively engaged at ATF3-bound sites that suppress Toll-like receptor signal

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

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

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

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

96 +) (macrophage) labeling, but no increase in ATF3(+) cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 Tumor ATF3 deletion improves the effect of ADORA1 antagonist t

113 ATF3 deletion was associated with increased lipopolysacc

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

115 s DNAJB1 and HSPA6 were found to be critical ATF3-dependent genes that elicited the antitumor respons

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

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

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

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

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

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

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

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

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

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

126 Conversely, knockdown of ATF3 exacerbates dendritic beading.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 Induction of ATF3 expression increases transcription throughout the A

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

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

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

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

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

148 UVA induced ATF3 expression through reactive oxygen species-mediated

149 Restoring ATF3 expression under NF-kappaB1 knockdown conditions re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 gh conditional targeting of TFs that include ATF3, GR, and PREP1.

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

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

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

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

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

172 that HSF1 is transcriptionally controlled by ATF3 in response to classic stimuli that promote heat ge

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 urthermore, functional assays disclosed that ATF3 is necessary and sufficient for HSF1 regulation.

194 ailed gene expression analysis revealed that ATF3 is one of the most highly induced ATFs in thermogen

195 Atf3 is required for negative feedback regulation of oth

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 miR-148a for modulating USP33 and downstream ATF3 levels in human microglial cells and contributes in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 pression abolished the inhibitory effects of ATF3 on invasion.

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

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

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

242 ATF3 overexpression in AK4-overexpressing cells limits i

243 s prominently (P = 6.2 x 10(-13)), including Atf3 (P = 2.4 x 10(-41)), Penk (P = 1.3 x 10(-15)), and

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

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

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

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

248 Accordingly, ATF3 promoted the expression of the metastasis suppresso

249 The TA treatment also induced ATF3 promoter activity.

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

251 ine 27 and histone 3 lysine 18) flanking the ATF3 promoter region.

252 creased RNA polymerase II recruitment to the ATF3 promoter, a synergistic upregulation of ATF3, and a

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

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

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 in turn decreases the stability of cellular ATF3 protein via deubiquitylation.

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

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

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

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

263 ATF3 repressed mutp53-induced NFKB2 expression and sensi

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

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

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

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

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

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

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

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

285 1 ATF/CRE and ACM sequences to bind ATF4 and ATF3 using immunoblot-EMSA and confirmed ATF4, ATF3, and

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

287 ATF3 was highly induced by combined PDI and HDACi treatm

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

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

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

291 ATF3 was then induced and bound to cytokine gene promote

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

293 ed that cAMP-dependent transcription factor (ATF3) weakly binds to the CH25H promoter, suggesting coo

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

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

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

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

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

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

300 nal networks controlled by CREB5, FOXD1, and ATF3, which suppress the activity of MAPK-mediated signa