ライフサイエンスコーパス: ATF4

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

2 lation of activating transcription factor 4 (Atf4).

3 ulated by activating transcription factor 4 (ATF4).

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

5 ession of Activating Transcription Factor-4 (ATF4).

6 on of eIF2alpha promotes mRNA translation of Atf4.

7 itically depends on the transcription factor Atf4.

8 UPR genes, and in particular ERN1 (IRE1) and ATF4.

9 e coding variation in the eIF2alpha effector ATF4.

10 diated by the transcription factors CHOP and ATF4.

11 a and PERK and reduced induction of CHOP and ATF4.

12 t is dependent on both MEK/ERK signaling and ATF4.

13 t whose expression is directly controlled by ATF4.

14 lasmic reticulum UPR pathway, independent of ATF4.

15 in the induction of the transcription factor ATF4(1-3).

16 show that Activating Transcription Factor 4 (ATF4), a DISC1 binding partner, is more abundant in the

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

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

19 ATF4, a key transcription mediator of the integrated str

20 throblasts, we identify transcription factor ATF4, a known HRI-regulated protein, as a novel gamma-gl

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

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

23 This occurs through MYCN and ATF4 activation of the SGOC biosynthetic pathway in MYCN

24 in response (UPR) in Drosophila We show that ATF4 activation reprograms nuclear gene expression and c

25 f ER stress in renal tubular cells with ATF3/ATF4 activation.

26 that chromatin accessibility is critical for ATF4 activity at the ASNS promoter, which can switch ALL

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

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

29 ar translocation of the transcription factor ATF4 also occurred, which normally drives expression of

30 Mechanistically, UHMK1 activated ATF4, an important transcription factor in nucleotide sy

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

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

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

34 more, one of these heterodimers, composed of ATF4 and CCAAT enhancer-binding protein beta (C/EBPbeta)

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

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

37 and ER stress-related (p-PERK, p-eIF2alpha, ATF4 and CHOP) apoptotic pathways.

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

39 ATF4 and FAM129A protein expression is increased in pati

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

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

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

43 pregulating its downstream effector proteins ATF4 and GADD45alpha.

44 intermediates, provided novel insights into ATF4 and GCN4 mRNA translational control, and demonstrat

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

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

47 Myt1 binds putative enhancers of Atf4 and Hsps, whose overexpression largely recapitulate

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

49 t one of the canonical UPR branches, through ATF4 and its target gene FAM129A, is required for PCa gr

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

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

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

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

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

55 s, and our further examination revealed that ATF4 and PERK regulated autophagy through separate mecha

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

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

58 tion through potential downstream control of ATF4 and SMAD4 to regulate target gene expression for ce

59 bition attenuates translational induction of ATF4 and the expression of its target asparagine synthet

60 gnificantly enhanced the binding of NCOA3 to ATF4 and the expression of purine metabolism-associated

61 ointly regulated by the transcription factor ATF4 and the nuclear receptor PPARalpha, which participa

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

63 phosphorylation and enhanced the activity of ATF4 and UHMK1.

64 nesis of endothelial cells through elevating ATF4 and VEGF.

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

66 enes activating transcription factors (e.g., Atf4) and heat-shock proteins (Hsps).

67 effector activating transcription factor 4 (Atf4) and induction of the ISR transcriptional program,

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

69 factors: activating transcription factor 4 (ATF4) and nuclear factor of activated T cells (NFAT).

70 ckdown of activating transcription factor 4 (ATF4) and overexpression of exogenous ATF4 cDNA indicate

71 levels of activating transcription factor 4 (ATF4) and phosphorylated eukaryotic translation initiati

72 ess sensor that can mediate the induction of ATF4, and calcineurin, a calcium-dependent regulator of

73 aling pathway consisting of PERK, eIF2alpha, ATF4, and GADD45alpha.

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

75 2alpha (eIF2alpha), the transcription factor ATF4, and the heat shock protein HSPB8.

76 ed kinase Perk and a subsequent induction of Atf4; and directly represses the expression of T-bet, a

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

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

79 ereas IRE1 is a negative regulator, PERK and ATF4 are required at distinct steps in the autophagic pa

80 Our results establish ATF4 as a cellular rheostat of MYC activity, which ensur

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

82 We identify ATF4 as differentially expressed in P47 and S47 cells an

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

84 n neurons activates the transcription factor ATF4 as part of the endoplasmic reticulum unfolded prote

85 dentified activating transcription factor 4 (ATF4) as a novel regulator of fetal gamma-globin gene ex

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

87 1 (Nupr1), a stress response gene induced by ATF4, as the gene most strongly upregulated.

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

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

90 The PERK-eIF2alpha-ATF4 axis increases supercomplex assembly factor 1 (SCAF

91 uggest that targeting the TGF-beta(1)-mTORC1-ATF4 axis may represent a novel therapeutic strategy for

92 -2 dependence and the 'primed' state via the ATF4-BIM/NOXA axis.

93 ATF4 binding motifs are identified in multiple clock gen

94 Increased Atf4 binding regulated the association of elongation fac

95 1-ATF4 interaction, and results in excessive ATF4 binding to DNA targets and deregulated gene express

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

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

98 Finally, ChIP assays verified an ATF4-binding site in the LAMP3 gene promoter, and a dual

99 a dual-luciferase assay confirmed that this ATF4-binding site is indeed required for transcriptional

100 ATF4 binds to the TTGCAGCA motif in the Per2 promoter an

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

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

103 BCB1 through remodeling and activation of an ATF4-bound, stress-responsive enhancer.

104 diated by activating transcription factor 4 (ATF4) but are accompanied by activation of nuclear facto

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

106 MYC upregulates ATF4 by activating general control nonderepressible 2 (G

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

108 This three-way interaction between ATF4, C/EBPbeta, and the ATF-C/EBP composite site activa

109 Within skeletal muscle fibers, the ATF4-C/EBPbeta heterodimer interacts with a previously u

110 expressed in P47 and S47 cells and show that ATF4 can reverse the redox status and rescue metabolism

111 ulated by atfs-1, the C. elegans ortholog of ATF4, causing hypersensitivity to rotenone, which was re

112 tor 4 (ATF4) and overexpression of exogenous ATF4 cDNA indicated that ATF4 up-regulates LAMP3 mRNA le

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

114 f IRE1alpha and PERK, decreases induction of ATF4, CHOP, and XBP-1 and upregulates UPR target genes.

115 Only the elf2alpha-ATF4-CHOP pathway was regulated under these conditions.

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

117 MitoROS and ATF4-CHOP were blocked by MitoTEMPO, a mitochondrial ant

118 Moreover, ATP13A2 knockdown induced an ATF4-CHOP-dependent stress response following rotenone e

119 hese studies indicate a pathological role of ATF4-CHOP-GADD34 pathway in glaucoma and provide a possi

120 ic endoplasmic reticulum (ER) stress-induced ATF4-CHOP-GADD34 pathway is activated in TM of human and

121 c depletion or pharmacological inhibition of ATF4-CHOP-GADD34 pathway prevents TM cell death and resc

122 ed protein synthesis along with induction of ATF4-CHOP-GADD34 pathway.

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

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

125 Subsequently, ATF4 co-occupies promoter regions of over 30 MYC-target

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

127 igh-resolution atomic structure of the DISC1-ATF4 complex, we show that mechanistically, the mutation

128 Specifically, whereas ATF4 controlled transcription and was essential for auto

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

130 coincident with preferential translation of ATF4 (CREB2).

131 Knocking down ATF4 decreased NRF2 expression and its nuclear transloca

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

133 and inhibition of mTORC1 signalling rescues ATF4-deficient cells from MYC-induced endoplasmic reticu

134 ATF4-deficient human fibrosarcoma cells were unable to c

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

136 promoter, which can switch ALL cells from an ATF4-dependent adaptive response to ATF4-independent apo

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

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

139 Mitochondrial stress causes an ATF4-dependent increase in the level of the metabolite L

140 e induction of cyclooxygenase 2 (COX2) in an ATF4-dependent manner.

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

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

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

144 egulation of LAMP3 These results reveal that ATF4 directly regulates LAMP3, representing the first id

145 ATF4 directly stimulates transcription of BCL11A, a repr

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

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

148 ion of serine biosynthesis through an mTORC1/ATF4-driven pathway.

149 rvival and upregulated pathways dominated by ATF4-driven stress and proapoptotic responses.

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

151 A (FAM129A), which is critical in mediating ATF4 effects on prostate tumorigenesis.

152 tivates the xCT promoter in synergy with the ATF4 endoplasmic reticulum stress-associated transcripti

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

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

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

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

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

158 ase in eIF2alpha (Ser51) phosphorylation and ATF4 expression and to an increase in S6K1 (Thr389) phos

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

160 5MP overexpression also induces ATF4 expression in Drosophila The knockdown of 5MP1 in f

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

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

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

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

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

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

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

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

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

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

171 mportantly, in vivo therapeutic silencing of ATF4-FAM129A axis profoundly inhibited tumor growth in a

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

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

174 fibers in vivo Interestingly, we found that ATF4 forms at least five distinct heterodimeric bZIP tra

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

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

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

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

179 her, these results suggest a model of mTORC1-ATF4 hyperactivation and impaired lysosomal acidificatio

180 Functionally, overexpressing ATF4 in control neurons recapitulates deficits seen in D

181 ity of the Gcn4 transcription factor (called ATF4 in mammals), which facilitates the supply of metabo

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

183 For example, during amino acid limitations, ATF4 in the amino acid response induces expression of as

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

185 Expression of ATF4 in TM promotes aberrant protein synthesis and ER cl

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

187 ession of activating transcription factor 4 (ATF4) in skeletal muscle fibers.

188 role for activating transcription factor 4 (ATF4) in survival following MYC activation.

189 ATF4, in turn, promoted the transcription of genes encod

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

191 from an ATF4-dependent adaptive response to ATF4-independent apoptosis during asparagine depletion.

192 to asparagine deficiency, which facilitates ATF4-independent induction of CCAAT-enhancer-binding pro

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

194 ts identify a biochemical mechanism by which ATF4 induces skeletal muscle atrophy, providing molecula

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

196 ATF3 and ATF4 induction downregulated Klotho through altered tran

197 ification of two critical regulators of such ATF4 induction, the noncanonical initiation factors eIF2

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

199 tivation of GCN2 and subsequent induction of ATF4, inhibition of mTORC1, proliferation arrest, and ce

200 e molecular and structural basis of an DISC1-ATF4 interaction underlying transcriptional and synaptic

201 the mutation of DISC1 disrupts normal DISC1-ATF4 interaction, and results in excessive ATF4 binding

202 ATF4 interacts with CHOP and this interaction is essenti

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

204 ATF4 is a member of the basic leucine zipper transcripti

205 ATF4 is a pro-oncogenic transcription factor whose trans

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

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

208 ion factors are obligate dimers, and because ATF4 is unable to form highly-stable homodimers, we hypo

209 ever, how mitochondrial stress is relayed to ATF4 is unknown.

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

211 s of UPR, activating transcription factor 4 (ATF4), is essential for prostate cancer (PCa) growth and

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

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

214 nt neurons with CRISPR-mediated heterozygous ATF4 knockout.

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

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

217 ty to increase eIF2alpha phosphorylation and ATF4 levels.

218 ghly-stable homodimers, we hypothesized that ATF4 may promote muscle atrophy by forming a heterodimer

219 s metastasis, inflammatory signaling, and an ATF4-mediated feedback loop that maintains de-differenti

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

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

222 ression of human eIF2gamma-I259M derepressed ATF4 messenger RNA translation in human cells.

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

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

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

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

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

228 tion with activating transcription factor 4 (ATF4), modifies gene expression patterns upon T. gondii

229 ain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely disp

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

231 s paradoxically stimulate the translation of ATF4 mRNA through a regulatory 5' leader sequence with m

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

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

234 lation of activating transcription factor 4 (ATF4) mRNA.

235 stress, and developmental defects similar to ATF4 mutants.

236 state levels of Fe-S clusters and normalizes ATF4, NRF2, and IRP2 signaling events associated with FR

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

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

239 Silencing ATF4 or CCT3 inhibited the selection and growth of TRCs

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

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

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

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

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

245 Additionally, the HRI-eIF2alphaP-ATF4 pathway represses mechanistic target of rapamycin c

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

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

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

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

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

251 involved and showed that TGF-beta(1)-induced ATF4 production depended on cooperation between canonica

252 r, the direct biochemical mechanism by which ATF4 promotes muscle atrophy is unknown.

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

254 and DENR deficient human cells show impaired ATF4 protein induction in response to ER stress.

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

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

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

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

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

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

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

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

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

269 Acute deletion of ATF4 significantly delays MYC-driven tumour progression

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

271 molecules in the selection of TRCs, such as ATF4, SLC3A2, CCT3, and hsa-miR-199a-5p.

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

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

274 eomic analyses, we identified a novel direct ATF4 target gene, family with sequence similarity 129 me

275 Importantly, ATF4 target genes are activated during iron deficiency t

276 Furthermore, ATF4 target genes are most highly activated during iron

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

278 the dimerization- and DNA-binding domain of ATF4 (the bZIP domain) in mouse skeletal muscle fibers i

279 uction of activating transcription factor 4 (ATF4), the transcriptional master regulator of amino aci

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

281 cover a linear signaling pathway from HRI to ATF4 to BCL11A to gamma-globin and illustrate potential

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

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

284 a set of 13 TFs (STAT1, IRF1, HIF1A, STAT4, ATF4, TP63, EGR1, CDKN2A, RBL1, E2F1, PRDM1, GATA3, and

285 pha (Ser51), and an increase in the level of ATF4 transcription factor.

286 In addition, DELE1 is required for ATF4 translation downstream of eIF2alpha phosphorylation

287 g motif for regulation of 5' leader-mediated ATF4 translation.

288 hat eIF2D and DENR are critical mediators of ATF4 translational induction and stress responses in viv

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

290 ession of exogenous ATF4 cDNA indicated that ATF4 up-regulates LAMP3 mRNA levels.

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

292 Strikingly, ATF4 was activated independently of PERK in both LNCaP a

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

294 ATF4 was not translated during hyperosmotic stress despi

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

296 m factor, activating transcription factor 4 (ATF4), were crucial for this induction, but surprisingly

297 lornithine (DFMO) also increased MitoROS and ATF4 when ATP13A2 was deficient.

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

299 vation of activating transcription factor 4 (ATF4), which was mediated by mammalian target of rapamyc

300 ion factor of the integrated stress response ATF4, which bound directly to the IL-8 promoter.