ライフサイエンスコーパス: ATF4

1 ulated by activating transcription factor 4 (ATF4).

2 , such as activating transcription factor 4 (ATF4).

3 t involve activating transcription factor 4 (ATF4).

4 lpha) and activating transcription factor 4 (ATF4).

5 including activating transcription factor 4 (ATF4).

6 on of the Activating Transcription Factor 4 (ATF4).

7 lation of activating transcription factor 4 (Atf4).

8 diated by the transcription factors CHOP and ATF4.

9 esses, but induces specific proteins such as ATF4.

10 expression of GADD34, a downstream target of ATF4.

11 DAC4 in the nucleus and its association with ATF4.

12 proteins including the transcription factor ATF4.

13 2alpha and promotes XIAP degradation through ATF4.

14 tion of DISC1 with the PDE4D9 locus requires ATF4.

15 silencing blocked the protective capacity of ATF4.

16 iation, and down-regulates the expression of ATF4.

17 of ATF5 is directly induced by both CHOP and ATF4.

18 ed translation of specific messages, such as ATF4.

19 itically depends on the transcription factor Atf4.

20 e coding variation in the eIF2alpha effector ATF4.

21 ession of activating transcription factor 4 (ATF4), a master transcription factor for stress-induced

22 hown that activating transcription factor 4 (ATF4), a master transcriptional effector of the ISR, pro

23 sm by the activating transcription factor 4 (ATF4), a member of the basic leucine zipper-containing p

24 he ISR is activating transcription factor 4 (ATF4), a transcription factor that regulates genes invol

25 criptome analysis demonstrated activation of ATF4, a key transcription factor in the integrated stres

26 ATF4, a key transcription mediator of the integrated str

27 coincident with preferential translation of ATF4, a transcriptional activator of the integrated stre

28 Upon loss of attachment, ATF4 activated a coordinated program of cytoprotective a

29 Instead, ATF4 activates the expression of cytoprotective genes, w

30 The transcription factor ATF4 (activating transcription factor 4) is induced by m

31 al agents and/or lead compounds for reducing ATF4 activity, weakness, and atrophy in aged skeletal mu

32 expression of negative transcription factor ATF4 (aka CREB2) both in human and a mouse model express

33 st development by upregulating the levels of ATF4, ALP and RUNX2, and it stimulated angiogenesis of e

34 A rescue of AAR activation in the absence of Atf4 also occurred for the Atf3 and C/EBP homology prote

35 SC1 inhibits the transcriptional activity of ATF4, an effect that is weakened by both 37W and 607F in

36 the CHAC1 ATF/CRE and ACM sequences to bind ATF4 and ATF3 using immunoblot-EMSA and confirmed ATF4,

37 with the bZIP domains from human JUN, XBP1, ATF4 and ATF5.

38 pression of activating transcription factors ATF4 and ATF6.

39 ess, the UPR-activated transcription factors ATF4 and ATF6alpha transcriptionally up-regulate Zip14 e

40 nse, manifested by enhanced transcription of ATF4 and C/EBP homologous protein.

41 on, together with corresponding decreases in ATF4 and CAAT/enhancer binding protein homologous protei

42 ctivated the unfolded protein response, both ATF4 and CHOP activation were diminished in Bok(-/-) cel

43 m induction of the UPR transcription factors ATF4 and CHOP by a mechanism involving increased express

44 Forced expression of ATF4 and CHOP protein before UVB irradiation significant

45 s, UPR proteins (GRP78, p-PERK, p-eIF2alpha, ATF4 and CHOP) and apoptosis were observed in PAO-treate

46 d the induction of UPR transcription factors ATF4 and CHOP, suggesting that the UPR could be targeted

47 hdrawal induced the stress response proteins ATF4 and CHOP/GADD153; however, LPS stimulation rapidly

48 rib3 is induced by the transcription factors ATF4 and CHOP; and downstream, Trib3 interferes with the

49 ng associated with increased p-eIF2alpha and ATF4 and decreased sXBP1 and CHOP.

50 bility of glucagon plus insulin to stimulate ATF4 and FGF21 expression.

51 imicked the ability of glucagon to stimulate ATF4 and FGF21 expression.

52 aling activity suppressed CDCA regulation of ATF4 and FGF21 expression.

53 resistance and tumor metastasis and suggest ATF4 and HO-1 as potential targets for therapeutic inter

54 Meanwhile, the increased expression of ATF4 and HO-1 mRNAs were observed in lesions derived fro

55 thways dependent on the transcription factor ATF4 and identified nuclear protein transcriptional regu

56 kers with COPD that may be driven in part by ATF4 and is modifiable with therapy.

57 ncrease in the transcriptional activation of ATF4 and NFATc1 genes.

58 Here, we show that UPR induces Sestrin2 via ATF4 and NRF2 transcription factors and demonstrate that

59 tarvation induces SLC7A11 expression through ATF4 and NRF2 transcription factors and, correspondingly

60 ucing direct transcriptional upregulation of ATF4 and other UPR genes.

61 echanisms by which HIF1alpha intersects with ATF4 and p53 pathways.

62 Loss of HIF1alpha resulted in activation of ATF4 and p53, the latter inhibiting CM proliferation.

63 n addition, activation of the GCN2-eIF2alpha-ATF4 and PERK-eIF2alpha-ATF4 signaling pathways are resp

64 ssion of eIF5 and 5MP induces translation of ATF4 and potentially other genes with uORFs in their mRN

65 protein response, with increases in Bip and ATF4 and reductions in spliced Xbp1 mRNA.

66 Despite this, a direct link between ATF4 and the degree of proliferative retinopathy has not

67 was the result of simultaneous activation of ATF4 and the transcription factor NRF2, which converged

68 nesis of endothelial cells through elevating ATF4 and VEGF.

69 We induced OIR in C57BL/6, ATF4(+/-), and endoplasmic reticulum stress-activated in

70 signals, activating transcription factor 4 (ATF4) and ATF6 indicating potential contributions of the

71 , such as activating transcription factor 4 (ATF4) and C/EBP-homologous protein (CHOP), that serve to

72 n of both activating transcription factor 4 (ATF4) and CHOP (DDIT3), critical regulators of the pathw

73 lation of activating transcription factor 4 (ATF4) and is a crucial evolutionarily conserved adaptive

74 ession of activating transcription factor 4 (ATF4), and cleavage of ATF6 were significantly increased

75 f cell stress pathways, including HIF1alpha, ATF4, and p53, are key to normal development and play cr

76 ing and a complex interplay among HIF1alpha, ATF4, and p53.

77 steoblastic markers (Runx2,Col1a1,Bglap2,Sp7,Atf4, andAlpl).

78 Furthermore, both 5MP and ATF4 are essential for larval development.

79 for the first time that both eIF2alphaP and ATF4 are necessary to promote erythroid differentiation

80 we show that the activation of the eIF2alpha/ATF4 arm of the unfolded protein response is sufficient

81 c-Myc and N-Myc activated the PERK/eIF2alpha/ATF4 arm of the UPR, leading to increased cell survival

82 These results elucidate ATF4 as a critical mediator of age-related muscle weakne

83 ranslation in neurodegeneration and identify ATF4 as a mediator for the spread of AD pathology.

84 Based on this finding, we investigated ATF4 as a potential mediator of age-related muscle weakn

85 Our study validates ATF4 as a prospective therapeutic target to inhibit neov

86 alpha, is a direct transcriptional target of ATF4 as is shown in ChIP assays.

87 dentified activating transcription factor 4 (ATF4) as a potential transcriptional regulator of genes

88 identify activating transcription factor 4 (ATF4) as the main regulator of the stress response.

89 1 (Nupr1), a stress response gene induced by ATF4, as the gene most strongly upregulated.

90 C/EBPgamma and ATF4 associate with genomic CAREs in a mutually dependen

91 hysically interacted with and phosphorylated ATF4 at tyrosine and threonine residues.

92 ression of vimentin, a negative regulator of ATF4, at the post-transcriptional level.

93 and ATF3 using immunoblot-EMSA and confirmed ATF4, ATF3, and CCAAT/enhancer-binding protein beta bind

94 by translation initiation inhibition and the ATF4/ATF3 pathway, and U bodies rapidly disappeared upon

95 In this study, we identify a novel DISC1 and ATF4 binding region in the genomic locus of phosphodiest

96 Increased Atf4 binding regulated the association of elongation fac

97 ed by two activating transcription factor 4 (ATF4) binding sites in the FGF21 gene.

98 ds to rapid expression of genes regulated by ATF4-binding cis elements.

99 PH oxidase-4 (Nox4) is induced downstream of ATF4, binds to a PP1-targeting subunit GADD34 at the end

100 Upstream of Atf4, BMP2 activates mTORC1 to stimulate protein synthes

101 eoblast differentiation genes osterix (Sp7), Atf4, bone sialoprotein (Ibsp), and osteocalcin (Bglap)

102 nce of unfolded protein response activation, ATF4 bound to the human VEGFA promoter and activated its

103 sulted from activation of the GCN2/eIF2alpha/ATF4 branch of the ISR pathway.

104 escued by an shATF4-resistant active form of ATF4, but not by a mutant that lacks transcriptional act

105 ver, for those genes with a downstream CARE, Atf4, C/ebp-homology protein (Chop), Pol II and TATA-bin

106 of SM hydrolysis partially protected against ATF4/C/EBP homology protein induction because of palmita

107 In this report, we further defined the ATF4-CHAC1 interaction by cloning the human CHAC1 promot

108 tion of unfolded protein response components ATF4, CHOP, GRP78, and XBP1 in CP.

109 a UPR effector signaling involving the PERK-ATF4-CHOP pathway, upregulation of the proapoptotic cell

110 K (protein kinase-like kinase) and eIF2alpha-ATF4-CHOP signaling.

111 hese findings indicate that the induction of ATF4/CHOP expression occurs via mTORC1 regulation of c-M

112 IF2alpha and thereby inhibit the p-eIF2alpha/ATF4/CHOP pro-apoptotic pathway, identifying miR-30b-5p

113 under ER stress, suppresses the p-eIF2alpha/ATF4/CHOP pro-apoptotic pathway.

114 anscription under conditions of ER stress or ATF4 coexpression: the -267 ATF/cAMP response element (C

115 Finally, 5MP and the paired uORFs allowing ATF4 control are conserved in the entire metazoa except

116 Here, we show that ATF4 controls a hepatic gene expression profile that ove

117 coincident with preferential translation of ATF4 (CREB2).

118 Knocking down ATF4 decreased NRF2 expression and its nuclear transloca

119 ctive of this study was to determine whether ATF4 deficiency could reduce neovascularization in mice

120 reconstitution of ATF4 or HO-1 expression in ATF4-deficient cells blocked anoikis and rescued tumor l

121 ATF4-deficient human fibrosarcoma cells were unable to c

122 In naive ATF4-deficient mice, we also observed an elevation in UP

123 kinase activity was required to inhibit the ATF4-dependent activation of the NOXA gene because the s

124 hese results establish HO-1 as a mediator of ATF4-dependent anoikis resistance and tumor metastasis a

125 ted adaptation and induces apoptosis through ATF4-dependent expression of pro-apoptotic factors inclu

126 ng intermediate filament protein, suppresses ATF4-dependent osteocalcin (Ocn) transcription and osteo

127 Inhibition of FASN induced an ATF4-dependent transcriptional induction of REDD1; downr

128 tryptophan 2,3-dioxygenase (TDO) resulted in ATF4-dependent upregulation of several amino acid transp

129 -transformed cells induces apoptosis through ATF4-dependent, but p53-independent, PUMA and NOXA induc

130 ATF4 depletion decreases both cell-density-dependent tra

131 ATF4 depletion preferentially attenuated hepatic lipogen

132 nto the underlying mechanism, we showed that ATF4 depletion resulted in a significant reduction in he

133 BPgamma:ATF4 heterodimers, but not C/EBPbeta:ATF4 dimers, are the predominant CARE-binding species in

134 Protein pull-down assays indicated that Atf4 directly interacts with CDK9 and its associated pro

135 In earlier studies, we showed that ATF4 down-regulation affects post-synaptic development a

136 Here, we find that ATF4 down-regulation in both hippocampal and cortical ne

137 screen showed that the transcription factor ATF4 drives ULBP1 gene expression in cancer cell lines,

138 nd phosphorylation-dependent inactivation of ATF4 during the pathogenesis of medullary thyroid cancer

139 In neuronal PC12 cells, silencing of ATF4 enhanced cell death in response to either 6-OHDA or

140 eby promoting translation of GCN4, the yeast ATF4 equivalent.

141 nase/activating transcription factor 4 (PERK/ATF4) ER stress pathway, innate immune mediators, and in

142 knockdown of 5MP1 in fibrosarcoma attenuates ATF4 expression and its tumor formation on nude mice.

143 increases FGF21 transcription by stimulating ATF4 expression and that activation of cAMP/PKA and PI3K

144 lic acid (CDCA) induced a 6-fold increase in ATF4 expression and that knockdown of ATF4 expression su

145 mycin to prevent bortezomib-induced CHOP and ATF4 expression as well as apoptosis.

146 R can induce tumor cell death, modulators of ATF4 expression could prove to be clinically useful.

147 and 5MP2, the second human paralog, promotes ATF4 expression in certain types of human cells includin

148 5MP overexpression also induces ATF4 expression in Drosophila The knockdown of 5MP1 in f

149 supporting a role for Fh1 in the control of Atf4 expression in mammals.

150 PKRi) demonstrate a significant reduction in ATF4 expression levels 3 h after one injection of PKRi.

151 Knocking down PERK or ATF4 expression or inhibiting PERK kinase activity dimin

152 that a targeted reduction in skeletal muscle ATF4 expression reduces age-related deficits in skeletal

153 ase in ATF4 expression and that knockdown of ATF4 expression suppressed the ability of CDCA to increa

154 in ATF4 protein abundance, and knockdown of ATF4 expression suppressed the ability of glucagon plus

155 tain ApoB100 protein levels independently of Atf4 expression, whereas hydrogen sulfide production is

156 ction of GCN2/eIF2alpha phosphorylation, and ATF4 expression, which overrides PERK/Akt-mediated adapt

157 iates the effect of glucagon plus insulin on ATF4 expression.

158 2alpha phosphorylation, dramatically delayed ATF4 expression.

159 al libraries were screened for modulators of ATF4 expression.

160 tially by an eIF2alpha-dependent increase in ATF4 expression.

161 onally to activating transcription factor 4 (ATF4) following treatment with oxidized phospholipids, a

162 and reveals a requirement for expression of ATF4 for expression of genes involved in oxidative stres

163 ied transcription factor for PTH and through ATF4 for the sympathetic tone.

164 pression and phosphorylation of Sestrin2, an ATF4 gene target, was increased by asparaginase, suggest

165 tectable effect upon stress-induced SNAT2 or ATF4 gene transcription, the associated increase in SNAT

166 crease in activating transcription factor 4 (ATF4) has been previously reported in the diabetic retin

167 Here, we show that C/EBPgamma:ATF4 heterodimers, but not C/EBPbeta:ATF4 dimers, are th

168 ctedly, without translation reprogramming an ATF4-high/MITF-low state is insufficient to drive invasi

169 es the ER stress markers CHOP, GADD45, EDEM, ATF4, Hsp90, ATG5, and phospho-eIF2alpha.

170 To explore the role of ATF4 in cell survival in PD-relevant contexts, we either

171 ontexts, we either silenced or overexpressed ATF4 in cellular models of PD.

172 Overexpression of GRP78 and ATF4 in human CP confirmed the experimental findings.

173 hospho-eIF2alpha independent upregulation of ATF4 in order to maintain ISR signaling, indicating that

174 otherapy, transcriptionally repress MITF via ATF4 in response to inhibition of translation initiation

175 However, the role of ATF4 in the pathogenesis of PD has not been explored.

176 ositioned Atf5 downstream of and parallel to Atf4 in the regulation of eIF4E-binding protein 1 (4ebp1

177 ISR and dose-dependently increased levels of ATF4 in transformed cells.

178 e role of activating transcription factor 4 (ATF4) in controlling the hepatic transcriptome and media

179 ression of ER stress markers such as Bip and Atf4, increased bone growth, and reduced skeletal dyspla

180 that the loss of function of either DISC1 or ATF4 increases PDE4D9 transcription, and that the associ

181 eated with tyrosine kinase inhibitors or the ATF4 inducer eeyarestatin as well as in RET-depleted TT

182 We showed recently that ATF4 induces an anabolic program through the up-regulati

183 In cultured cells, ATF4 induces transcriptional expression of genes directe

184 rylation, activating transcription factor-4 (ATF4) induction, and increased expression of known downs

185 did not directly regulate the expression of ATF4; instead, it enhanced the expression of vimentin, a

186 proteins, including GRP78, PERK, eIF2alpha, ATF4, IRE1alpha, JNK, p38, and CHOP.

187 ATF4 is a pro-oncogenic transcription factor whose trans

188 ATF4 is a transcriptional activator of the integrated st

189 and show in liver exposed to ER stress that ATF4 is not required for CHOP expression, but instead AT

190 RNA-Seq analysis indicates that ATF4 is responsible for a small portion of the PERK-depe

191 eostasis, activating transcription factor 4 (ATF4), is dysfunctional in HD because of oxidative stres

192 t Atf5, a close but less-studied relative of Atf4, is also a target of Pdx1 and is critical for beta-

193 IF2alphaP-activating transcription factor 4 (ATF4) ISR in primary erythroid precursors to combat oxid

194 six activator protein 1 (AP-1) transcripts (ATF4,JUNB,JUN,FOSB,FOS, andJUND) were up-regulated at d9

195 Induction of gamma-H2AX was abrogated in ATF4 knockdown cells.

196 characterize whole-body and tissue-specific ATF4-knockout mice and show in liver exposed to ER stres

197 ATF4 levels are also upregulated in neuronal PC12 cells

198 We find that ATF4 levels are increased in neuromelanin-positive neuro

199 marked decreases in p-PERK, p-eIF2alpha, and ATF4 levels but robust increases in GRP78 protein levels

200 ases eIF2alpha phosphorylation and HSP90 and ATF4 levels, and limits the accumulation of soluble Abet

201 lated kinase) phosphorylation, and HSP90 and ATF4 levels.

202 ty to increase eIF2alpha phosphorylation and ATF4 levels.

203 revealed DNA copy number alterations at the ATF4 locus, an important activator of the UPR/AAR pathwa

204 ATF4 may exert either protective or deleterious effects

205 pending on the extent of protein disruption, ATF4 may not be able to restore proteostatic control and

206 that mitochondrial DNA depletion leads to an ATF4-mediated increase in serine biosynthesis and transs

207 somal recessive PD, plays a critical role in ATF4-mediated protection.

208 pertonicity by a mechanism dependent on both ATF4-mediated transcription of the SLC38A2 gene and enha

209 etase genes downstream of the stress-induced ATF4-mediated transcription program.

210 Livers from Atf4 (-/-) or Atf4 (+/-) mice displayed an amplification of the amino

211 r explored selected responses in livers from Atf4 (+/-) mice.

212 rns in livers from wildtype, Gcn2 (-/-), and Atf4 (-/-) mice treated with asparaginase or excipient a

213 in hepatic mTORC1 signaling was retained in Atf4 (-/-) mice treated with asparaginase.

214 ective erythropoiesis of Hri(-/-) , eAA, and Atf4(-/-) mice by inhibiting both HRI and mTORC1 signali

215 ffect of ATF4 on hepatic lipid metabolism in Atf4(-/-) mice fed regular chow or provided with free ac

216 Of particular significance, we found that Atf4(-/-) mice, as opposed to wild-type littermates, wer

217 d excessive fat accumulation in the liver of Atf4(-/-) mice, when compared with wild-type littermates

218 ee key functions in the lipogenic pathway in Atf4(-/-) mice.

219 retrograde transport or knockdown of axonal Atf4 mRNA abolished Abeta-induced ATF4 transcriptional a

220 globin synthesis and enhances translation of ATF4 mRNA in mouse beta-thalassemic erythroid precursors

221 tor rescued memory impairment and attenuated ATF4 mRNA increased expression in the ApoE4 mice.

222 tionale for this discordant response is that ATF4 mRNA is reduced by UVB, and despite its ability to

223 Significance statement: ATF4 mRNA relative quantities are elevated in ApoE4 alle

224 Protein synthesis and Atf4 mRNA were upregulated in these axons, and coinjecti

225 bles translation of the transcription factor ATF4 mRNA.

226 lation of activating transcription factor 4 (ATF4) mRNA to induce stress response genes.

227 ced body size and microphthalmia, similar to ATF4-null animals.

228 tin immunoprecipitation assays revealed that ATF4 occupancy increased at the NOXA promoter in TT cell

229 We determined the effect of ATF4 on hepatic lipid metabolism in Atf4(-/-) mice fed r

230 However, expression of ATF4 or CHOP was not induced by UVB as compared with tra

231 for the UPR-associated transcription factors Atf4 or Chop were significantly protected from CNT, impl

232 ngs in a murine model, and reconstitution of ATF4 or HO-1 expression in ATF4-deficient cells blocked

233 scription factors and, correspondingly, that ATF4 or NRF2 deficiency also renders cancer cells more r

234 Livers from Atf4 (-/-) or Atf4 (+/-) mice displayed an amplification

235 t that inhibition of PKR is a way to restore ATF4 overexpression and memory impairment in early stage

236 with COPD-associated airway expression, and ATF4 overexpression in airway epithelial cells in vitro

237 e toxin-induced reduction of parkin, whereas ATF4 overexpression partially preserves parkin levels.

238 ovel antioxidant regulator and an obligatory ATF4 partner that controls redox homeostasis in normal a

239 e independent of the well characterized GCN2-ATF4 pathway and instead dependent on MEK-ERK signaling,

240 ith mitochondrial diseases, we show that the ATF4 pathway is activated in vivo upon mitochondrial str

241 Furthermore, the HRI-eIF2alphaP-ATF4 pathway suppresses mTORC1 signaling specifically in

242 ER stress, triggering activation of the PERK-ATF4 pathway, which potentially contributes to the lens

243 ogen sulfide production is promoted via GCN2-ATF4 pathway.

244 ta/delta and activation of the HRI-eIF2alpha-ATF4 pathway.

245 other things, an activation of the Nrf2 and ATF4 pathways.

246 These data demonstrate that ATF4 plays a critical role in regulating hepatic lipid m

247 These results indicate that ATF4 plays a protective role in PD through the regulatio

248 c-MYC subsequently bound to the ATF4 promoter, suggesting direct involvement of an mTORC

249 plus insulin stimulated a 5-fold increase in ATF4 protein abundance, and knockdown of ATF4 expression

250 ATF4 protein and transcripts were found with greater fre

251 that eIF2alphaP is required for induction of ATF4 protein synthesis in vivo in erythroid cells during

252 Conversely, overexpression of ATF4 reduced cell death caused by dopaminergic neuronal

253 s seen in an impairment of cell migration on ATF4 reduction in non-neuronal cells.

254 e identified a new cellular pathway in which ATF4 regulates the expression of RhoGDIalpha that in tur

255 phylogenetic and functional linkage between ATF4 regulation and 5MP expression in this group of euka

256 SCs and a novel cell-free assay reveals that ATF4 requires C/EBPbeta for genomic binding at a motif d

257 dant supplementation reverses the disordered ATF4 response to nutrient stress.

258 ith this pattern of gene expression, loss of ATF4 resulted in enhanced oxidative damage, and increase

259 The OIR ATF4(+/-) retinas demonstrated reprogramming of the UPR

260 ia-driven neovascularization in experimental ATF4(+/-) retinas.

261 rapidly phosphorylated Erk, and up-regulated Atf4, Runx2, Osx, Lrp5, beta-catenin, Alp, and Col1a1; t

262 GCN2 and ATF4 serve complementary roles in the hepatic response t

263 it inflammation and mTORC1 signaling whereas ATF4 serves to limit the amino acid response and prevent

264 asparaginase exposure is not driven via eIF2-ATF4-Sestrin2.

265 g hepatic activating transcription factor 4 (Atf4) showed an exaggerated ISR and greater loss of endo

266 We propose that the PERK/eIF2alpha-P/ATF4 signaling acts as a brake in the decline of protein

267 We report here that the PERK/eIF2alpha/ATF4 signaling branch of the integrated endoplasmic reti

268 heme deficiency in vivo, this HRI-eIF2alphaP-ATF4 signaling is necessary both to reduce oxidative str

269 f the GCN2-eIF2alpha-ATF4 and PERK-eIF2alpha-ATF4 signaling pathways are responsible for increased PE

270 lator of this response is the PERK/eIF2alpha/ATF4 signaling where eIF2alpha is phosphorylated (eIF2al

271 eIF2alpha/activating transcription factor 4 (ATF4) signaling module.

272 ession through an AKT-independent, PDK1-RSK2-ATF4 signalling axis.

273 and human tumor cell lines, and knockdown of ATF4 significantly increased the antiproliferative effec

274 (PERK) or activating transcription factor 4 (ATF4) significantly reduced the production of angiogenes

275 on of the transcription factor XBP1, but not ATF4, significantly delay locomotor recovery.

276 ATF4 silencing exacerbates the toxin-induced reduction o

277 regulated in these axons, and coinjection of Atf4 siRNA into the DG reduced the effects of Abeta1-42

278 ranscriptional regulators, including NFE2L2, ATF4, Srebf1 and Rictor were identified as potential key

279 at block threonine phosphorylation increased ATF4 stability and activated its targets NOXA and PUMA.

280 HRI-eIF2alphaP-ATF4 stress signaling is important not only to inhibit e

281 ption factors like C/EBPbeta, C/EBPdelta and ATF4 that have G/C rich or uORF sequences in their 5' UT

282 , primarily by the bZIP transcription factor ATF4 through its recruitment to cis-regulatory C/EBP:ATF

283 ranslational control of transcription factor ATF4 through paired upstream ORFs (uORFs) plays an impor

284 er recruitment of the bZip TFs C/EBPbeta and ATF4 to a non-canonical C/EBP DNA sequence.

285 ous amino acids, activated GCN2 up-regulates ATF4 to induce expression of the stress response protein

286 tiation of a transcriptional program through ATF4 to promote recovery from nutrient deprivation.

287 r characterize the interaction of DISC1 with ATF4 to show that it is regulated via protein kinase A-m

288 esis enzyme genes PHGDH, PSAT1 and SHMT2 via ATF4 to support glutathione and nucleotide production.

289 of axonal Atf4 mRNA abolished Abeta-induced ATF4 transcriptional activity and cell loss.

290 lly induced by phosphorylation of eIF2alpha, ATF4 translation can be also induced by expression of a

291 lammation-mediated hepatic processes whereas ATF4 uniquely associates with cholesterol metabolism and

292 nduced by activating transcription factor 4 (Atf4) via C/ebp-Atf-Response-Element (CARE) enhancers.

293 ATF4 was also protective against 6-OHDA-induced death of

294 ATF4 was further demonstrated to bind directly to cis-re

295 ATF4 was not translated during hyperosmotic stress despi

296 Levels of ATF4 were similar in wild type and heterozygous lenses b

297 ession of activating transcription factor 4 (Atf4), which indicates the activation of oxidative stres

298 on factor Activating Transcription Factor 4 (ATF4), which is involved in the regulation of cellular s

299 ulated by activating transcription factor 4 (ATF4), which was activated by mTORC1 independent of its

300 e AAR and UPR lead to increased synthesis of ATF4, which mediates PCK2 transcriptional up-regulation