ライフサイエンスコーパス: ATF

1 ATF, uPAR84-95, and WKYMVm regulated adhesion, migration

2 ATF-1 coinduces heme oxygenase-1 (HO-1) and Liver X rece

3 ATF-1 required phosphorylation for full functional activ

4 ATF-2 and p38 activation inhibit chondrocyte hypertrophy

5 ATF-2 knockdown blocked VEGF-A-stimulated VCAM-1 express

6 ATF-2 or SMAD-3, but not IRF-3, short-hairpin RNA reduce

7 ATF-2 was also required for other endothelial cell outpu

8 ATF-3 expression was quantified by using immunocytochemi

9 ATFs were transcriptionally distinct from bloodstream fo

10 uction of activating transcription factor 1 (ATF-1).

11 Active transcription factor-1 (ATF-1) was identified, and as this transcription factor

12 r responds to GADD45beta together with AP-1, ATF, or C/EBP family members.

13 ranscription factors, including Egr-1, AP-1, ATF-2, and NF-kappaB.

14 g protein (CREB)/ATF proteins (c-Jun, ATF-1, ATF-2, JunD, and CREB).

15 itation assays, we demonstrated that CREB-1, ATF-2, and c-Jun bound constitutively at the TGFbeta3 pr

16 -responsive element-binding protein (CREB)-1/ATF-1-like factors.

17 diated by activating transcription factor 2 (ATF-2) and (ii) H(2)O(2)-induced catalase expression thr

18 MAPK, and activating transcription factor 2 (ATF-2) in RA ST fibroblasts in a time-dependent manner,

19 otein and activating transcription factor 2 (ATF-2) to the cAMP-responsive element site was methylati

20 al factor activating transcription factor-2 (ATF-2) bound to ATF sites in the PTEN promoter.

21 The activating transcription factor-2 (ATF-2) mRNA encodes a member of the ATF/CRE-binding prot

22 c-Jun and activating transcription factor-2 (ATF-2) upon activation by a variety of stress-based stim

23 RK1/2 and activating transcription factor-2 (ATF-2).

24 response element (CRE) site and a novel -248 ATF/CRE modifier (ACM) element.

25 of ER stress or ATF4 coexpression: the -267 ATF/cAMP response element (CRE) site and a novel -248 AT

26 S-3), and activating transcription factor 3 (ATF-3), which terminate inflammatory responses in macrop

27 ry marker activating transcription factor 3 (ATF-3).

28 F-3 site and mutations at the IRF-3, SMAD-3, ATF-2, or NF-kappaB, but not the IRF-7, sites significan

29 ding BiP, activating transcription factor 4 (ATF-4), ATF-6, and a spliced form of X-box binding prote

30 regulator activating transcription factor 4 (ATF-4).

31 rylation (activating transcription factor 4 [ATF-4], C/EBP homologous transcription factor [CHOP], ox

32 , activating transcription factor 4 (ATF-4), ATF-6, and a spliced form of X-box binding protein 1, we

33 ownstream Activating Transcription Factor-7 (ATF-7).

34 sembly of the transcription factors IRF-3/7, ATF-2/c-Jun, and NF-kappaB on the ifnbeta promoter.

35 glucosylceramide or sphingomyelin, activated ATF-6 upon treatment with ER stress inducers tunicamycin

36 The activated ATF-2 translocated to the nucleus where it attached to i

37 mmon alpha-helical scaffold producing active ATFs.

38 Additionally, ATF-2 controls expression of CREB and c-Jun during T cel

39 ymerase chain reaction, Western blotting, an ATF-2 DNA-binding assay, and a p38 kinase activity assay

40 Our definition of an ATF-1-mediated pathway for linked protection from foam c

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

42 naling regulating the expression of Id-1 and ATF-3, thus contributing to melanoma metastasis.

43 reversed the expression patterns of Id-1 and ATF-3.

44 s the UPR pathway proteins IRE-1, XBP-1, and ATF-6.

45 recipitation assays revealed that SMAD-3 and ATF-2 bind to the endogenous p19 promoter in RAW264.7 ce

46 ifically, they neither up-regulate ATF-4 and ATF-4 targets nor suppress protein translation.

47 regulation of transcription by p300/CBP and ATF-2.

48 n expression and phosphorylation of CREB and ATF-1 transcription factors that were required for up-re

49 a positive transactivation role of c-Jun and ATF-2 but unexpectedly revealed a strong negative role o

50 ibitor 2 pretreatment blocks these c-Jun and ATF-2 phosphorylation increases.

51 cture and increased association of c-Jun and ATF-2.

52 diated P2Y2R-induced activation of c-Jun and ATF-2.

53 ation of the transcription factors c-Jun and ATF-3 (activating transcription factor 3), known regulat

54 involve the JNK substrates c-Jun, JunD, and ATF-2.

55 regulatory factor 3 (IRF-3), NF-kappaB, and ATF-2 in C(ko)-infected compared to V(ko) or parental vi

56 lated p300 HAT, suggesting that the loop and ATF-2 compete for p300 HAT binding.

57 ecent studies have identified peripherin and ATF-3 molecules as crucial for neurite outgrowth propaga

58 VIP quickly elevates CREB Ser133 and ATF-1 Ser63 phosphorylation levels, although the CREB Se

59 four TN-C isoforms in rat vascular SMCs, and ATF-4 knockdown inhibited PDGF-BB-inducible TN-C express

60 BP, HNF-1, CREB, as well as factors, such as ATF, AP-2, LEF-1, GATA and PAX-6, that had not yet been

61 nd its downstream signaling targets, such as ATF-2, thereby enhancing the activity of superoxide dism

62 454 sequencing with Conexio Genomics ASSIGN ATF 454 HLA genotyping software analysis to analyze sequ

63 tial role in the formation of the asymmetric ATF-2/c-Jun/PRDIV complex.

64 the ATF/cyclic AMP response element-binding (ATF/CREB) family of transcription factors, plays a cruci

65 Both ATF-2 overexpression and p38 activation repressed type X

66 ted by p38 kinase activation of ATF-2 and by ATF-2 regulation of MLCK gene activity.

67 ATF-1, and HO-1 and LXR-beta were induced by ATF-1 transfection.

68 p300 HAT is much more potently inhibited by ATF-2 b-ZIP.

69 We also examined the ability of the CHAC1 ATF/CRE and ACM sequences to bind ATF4 and ATF3 using im

70 In conclusion, ATF-1, via p38 MAP kinase activation, functions as a nov

71 We identified a conserved ATF site in the dp5 promoter that binds c-Jun and ATF2,

72 uires assembly of an enhanceosome containing ATF-2/c-Jun, IRF-3/IRF-7, and NFkappaB.

73 factor-kappaB, AP-1, Ets-1, Elk-1, SRF, CRE/ATF, and NFATc.

74 both the AP-1 and CRE-binding protein (CREB)/ATF proteins (c-Jun, ATF-1, ATF-2, JunD, and CREB).

75 ucer and activator of transcription 3, CREB, ATF-2, and p53 and activation of 37 transcription factor

76 These findings suggest that CREB, ATF-2, and c-Jun are recruited to the IFN-gamma proximal

77 pulldown assays, we demonstrated that CREB, ATF-2, and c-Jun, but not cyclic AMP response element mo

78 have identified a potential role for a CREB/ATF family member, X-box binding protein 1 (XBP-1), in t

79 nt types of transcriptional activators: CREB/ATF-type Atf1, C(2)H(2)zinc finger-type Rst2, and CBF/NF

80 asma cells may reflect redundancy among CREB/ATF family members or the involvement of other plasma ce

81 Members of the C/EBP, AP-1 and CREB/ATF bZIP subfamilies form homodimeric or heterodimeric c

82 tory pathway genes mediated by Xbp1 and Creb/ATF factors is a characteristic and necessary feature of

83 rotein/activating transcription factor (CREB/ATF) and AP-1 transcription factors on the proximal prom

84 ed both by sequence-specific binding of CREB/ATF and by DNA methylation of a CpG island.

85 decreased expression of the targets of CREB/ATF family, heat-shock factor 1, ATF6, SRF, and E2F1 tra

86 ponse program at the ER to activate the CREB/ATF transcription factors ATF3 and ATF4.

87 main; PYD, pyrin N-terminal homology domain; ATF, activating transcription factor; and PTEN, phosphat

88 nt regions of the human SOX2 promoter; each ATF is constructed such that it contains or lacks a supe

89 owed that CHOP was associated with the C/EBP-ATF composite site regions of the SNAT2, VEGF, and CAT-1

90 ds to enhanced ATF4 recruitment to the C/EBP-ATF response element (CARE) upstream of Promoter-1.

91 amino acid transporter 2), contains a C/EBP-ATF site that binds ATF4 and triggers increased transcri

92 SNAT2 genomic fragment containing the C/EBP-ATF site.

93 stress-induced regulation of specific C/EBP-ATF-containing genes, such as ASNS.

94 ough its recruitment to cis-regulatory C/EBP:ATF response elements (CAREs) together with a dimeric pa

95 hmania parasites activate the PERK/eIF2alpha/ATF-4 pathway in cultured macrophages and infected human

96 lease of ATF3 from its cAMP response element/ATF target site.

97 novirus-mediated HuR overexpression elevated ATF-2 mRNA and protein levels, whereas HuR silencing ren

98 onucleoprotein complexes with the endogenous ATF-2 mRNA and specifically bound to 3'-UTR of ATF-2 mRN

99 no neuronal or Schwann cell nuclei exhibited ATF-3 immunoreactivity.

100 ipper domain (b-ZIP) of transcription factor ATF-2 (also called CRE-BP1) can interact with the CBP HA

101 ation and expression of transcription factor ATF-4.

102 6, basic leucine zipper transcription factor ATF-like (Batf), and IL-21, and STAT5 deficiency greatly

103 he basic leucine zipper transcription factor ATF-like, Batf is important for IL-4 expression in Tfh c

104 ctivator of activating transcription factor (ATF) 2, and c-Jun-NH(2)-kinase, induces expression of Fo

105 ily members activating transcription factor (ATF) 2, ATF3, and ATF7.

106 ynthesis of activating transcription factor (ATF) 4 by a translational control mechanism.

107 partner of activating transcription factor (ATF) 4 in a yeast two-hybrid screen and confirmed their

108 F2alpha and activating transcription factor (ATF) 4, which is essential for Fgf21-induced expression.

109 bers of the activating transcription factor (ATF) family in survival of diffuse large B-cell lymphoma

110 OS, MAF and activating transcription factor (ATF) family proteins characterized by basic region and l

111 of the CREB/activating transcription factor (ATF) family, increases in expression in parallel with AV

112 tein (CREB)/activating transcription factor (ATF) site overlapping a CpG island.

113 zinc finger artificial transcription factor (ATF) to up-regulate the Maspin promoter in aggressive ov

114 4 to -581), activating transcription factor (ATF)-2 (nt -571 to -568), IRF-7 (nt -533 to-525), and NF

115 substrate, activating transcription factor (ATF)-2.

116 e-dependent activating transcription factor (ATF)-adenosine 3',5'-monophosphate (cAMP) response eleme

117 one or more activating transcription factor (ATF)/cyclic AMP response element binding protein (CREB)

118 Activating transcription factor (ATF)3 regulates the expression of inflammation-related g

119 eracts with activating transcription factor (ATF)4, a key component of the integrated stress response

120 modulator, activating transcription factor (ATF)6, which can induce genes that encode components of

121 l repressor activating transcription factor (ATF-3) in a STAT1-dependent manner, which correlated wit

122 e basic leucine zipper transcription factor, ATF-like (BATF) gene (Batf(-/-)) lack TH17 and follicula

123 r basic leucine zipper transcription factor, ATF-like (BATF) is important for CD4(+) Th17, Th9, and f

124 ation of basic leucine transcription factor, ATF-like (BATF), a transcription factor in the AP-1 fami

125 (basic leucine zipper transcription factor, ATF-like) and Bcl6, in part through epigenetic modificat

126 (basic leucine zipper transcription factor, ATF-like) and IRF4 (interferon-regulated factor 4) induc

127 (basic leucine zipper transcription factor, ATF-like), an AP-1 protein family factor, is required fo

128 tress pathways and the transcription factors ATF (activating transcription factor) and CREB (cyclic A

129 well as the downstream transcription factors ATF-2 and c-Jun.

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

131 Artificial transcription factors (ATFs) and genomic nucleases based on a DNA binding platf

132 Artificial transcription factors (ATFs) are potent synthetic biology tools for modulating

133 Artificial transcription factors (ATFs) are precision-tailored molecules designed to bind

134 neered two artificial transcription factors (ATFs) that contain Cys(2)His(2) zinc-finger DNA-binding

135 ced expression of the transcription factors, ATF-2 and c-Jun, which normally bind to the IFN-gamma pr

136 We have created six-finger ATFs to target two different 18 nt regions of the human

137 ly in the orientation that places the folded ATF-2 basic segment in the upstream half of this asymmet

138 As expected, double labeling for ATF-3, a marker of cell bodies with damaged axons, showe

139 assays identify a 10-bp region required for ATF-1 induction of UCP3 promoter activity.

140 nce experiments further supported a role for ATF-3 in suppression of MMP-1 expression.

141 se tissue, here termed adipose tissue forms (ATFs), can replicate and were capable of infecting a nai

142 inase signalling and comprise dimers of FOS, ATF and JUN proteins.

143 thermore, uPA or its aminoterminal fragment (ATF) can promote the exposure of the uPAR88-92 region.

144 and in complex with amino-terminal fragment (ATF) to 3.2 A.

145 calbindin prevented the Golgi fragmentation, ATF-6 activation, and apoptosis in response to CerS6/C(1

146 ChIP-seq analysis of the effector-free ATFs in MCF7 breast cancer cells identified thousands of

147 A simple adaptive transfer function (ATF) was developed.

148 out mediated at least in part by a Wnt11 --> ATF/CREB --> TGFbeta2 pathway is critical in regulating

149 approximately 95% of the cardiac neurons had ATF-3-immunoreactive nuclei.

150 is more efficiently retained by immobilized ATF-2 b-ZIP than hypoacetylated p300 HAT.

151 BB-induced migration was also compromised in ATF-4 null mEFs, and this effect was rescued by the addi

152 culture, there was a significant increase in ATF-3 transcript levels, and neurturin partially suppres

153 F-2 mRNA unstable and prevented increases in ATF-2 mRNA and protein.

154 at hyperosmotic stress elicited increases in ATF-2 phosphorylation through a novel Polo-like kinase 3

155 HAT lysine acetylation sites were mapped in ATF-2 b-ZIP.

156 Inhibition of AgNP15-induced ATF-6 degradation with Site-2 protease inhibitors comple

157 treatment augmented cAMP levels and induced ATF-1/CREB serine 63/133 phosphorylation in both B linea

158 as siRNA-mediated knockdown of CerS6 induced ATF-6 activation and apoptosis in multiple human cancer

159 bination of PDE3 and PDE4 inhibitors induced ATF-1/CREB serine 63/133 phosphorylation in T cells.

160 to mimic 3-isobutyl-1-methylxanthine-induced ATF-1/CREB phosphorylation.

161 ed the effect of hyperosmotic stress-induced ATF-2 phosphorylation.

162 mutants enhanced hyperosmotic stress-induced ATF-2 phosphorylation.

163 ering chromatin accessibility and inhibiting ATF and C/EBPbeta recruitment to key enhancer regions.

164 -binding protein (CREB)/ATF proteins (c-Jun, ATF-1, ATF-2, JunD, and CREB).

165 confirmed that upon P2Y2R activation, c-Jun, ATF-2, and Fra-1, but not the typical c-Fos, bound to th

166 etected by gel shift analysis include c-jun, ATF-2, fos-B, fra-1, and fra-2.

167 the demonstrable AP-1 components are c-jun, ATF-2, jun-B, and fos-B.

168 the level of phosphorylation of JNK, c-Jun, ATF-2, MKK4, and MKK7 were also determined at various ti

169 the activation of AP-1 complexes of the Jun/ATF-type as an important element controlling the growth

170 Mechanistically, ATF-6 activation was regulated by a concerted two-step p

171 38 MAP kinase prevents both hypoxia-mediated ATF-1 phosphorylation and UCP3 up-regulation.

172 articles encapsulating a chemically modified ATF mRNA resulted in inhibition of ovarian cancer cell g

173 smic HuR levels and that polyamine-modulated ATF-2 expression plays a critical role in regulating epi

174 t not cyclic AMP response element modulator, ATF-1, or c-Fos, bind to the proximal promoter of IFN-ga

175 activity in T cells with a dominant-negative ATF-2 peptide or with small interfering RNA markedly red

176 Neuturin also could reverse neuronal ATF-3 expression after its induction.

177 ophic factor (GDNF) also suppressed neuronal ATF-3 induction during culture.

178 le for Kruppel-like factor, MEF2C, ETS, NFY, ATF, E2F2, and NRF1 transcription factors in determining

179 vo was regulated by p38 kinase activation of ATF-2 and by ATF-2 regulation of MLCK gene activity.

180 tein can suppress noise in the activation of ATF-2 by separately inhibiting the TNF receptor complex

181 Activation of ATF-2 was JNK, but not p38 or ERK MAPK dependent.

182 eater amount of noise than the activation of ATF-2.

183 required p38 kinase-dependent activation of ATF-2.

184 ChIP analysis showed increased binding of ATF-3 to the Id-1 promoter after MUC18 silencing.

185 otein dimerization) domain characteristic of ATF/CREB proteins, but no other functional domains or cl

186 ism stimulating injury-induced expression of ATF-3 in cardiac neurons.

187 The injury-induced expression of ATF-3 was decreased in the DRG of fat-1 mice, whereas th

188 tra-articular 2 mg MIA induced expression of ATF-3, a sensitive marker for peripheral neuron stress/i

189 sion of the dominant-negative mutant form of ATF-6 protected cells from apoptosis in response to CerS

190 scriptional profiling, and identification of ATF binding sites reveal that the ATFs do not directly t

191 pha/Abeta-fibers and reduced the increase of ATF-3 and TRPV1 immunoreactivity in dorsal root ganglion

192 In 2-hour cultures, the induction of ATF-3 expression was evident in many Schwann cell nuclei

193 Inhibition of ATF-2 activity in T cells with a dominant-negative ATF-2

194 Furthermore, inhibition of ATF-2 expression prevented the increased resistance of p

195 osphorylation of ATF-1, and the knockdown of ATF-1 by shRNA prevents hypoxia-mediated up-regulation o

196 and LXR-beta were suppressed by knockdown of ATF-1, and HO-1 and LXR-beta were induced by ATF-1 trans

197 siRNA knockdown of ATF-6alpha in lung epithelial cells inhibited expression

198 luoromethylornithine increased the levels of ATF-2 mRNA and protein, whereas increasing polyamines by

199 st time that both mRNA and protein levels of ATF-4 are induced in smooth muscle cells (SMCs) by the p

200 Gene expression microarrays of ATF-transduced cells revealed an exceptional specificity

201 Overexpression of ATF-4 increased transcript levels of the four TN-C isofo

202 esis, associated with the phosphorylation of ATF-1 serine 63 and CREB serine 133, dependent on protei

203 Hypoxia promotes the phosphorylation of ATF-1, and the knockdown of ATF-1 by shRNA prevents hypo

204 anslocation was increased phosphorylation of ATF-2 on threonine residue 71 (T71).

205 manner, which correlated with recruitment of ATF-3 to the endogenous MMP-1 promoter as detected by ch

206 These data reinforce the role of ATF-1 as a hypoxia-responsive trans-activator and identi

207 Our findings thus demonstrate the role of ATF-4 in both injury- and PDGF-BB-inducible TN-C express

208 Small interfering RNA induced silencing of ATF-2, or mutation of the ATF-2 binding motif prevented

209 te that polyamines modulate the stability of ATF-2 mRNA by altering cytoplasmic HuR levels and that p

210 gene promoter but increased the stability of ATF-2 mRNA.

211 The suppression of ATF-3 induction by neurturin was mediated by activation

212 F-2 mRNA and specifically bound to 3'-UTR of ATF-2 mRNA on multiple nonoverlapping 3'-UTR segments.

213 ction of the 3'-untranslated region (UTR) of ATF-2 with cytoplasmic HuR.

214 network and discovered three combinations of ATFs capable of inducing pluripotency without exogenous

215 ed the first targeted, non-viral delivery of ATFs into tumors with potential clinical applications fo

216 Libraries of ATFs enable the high-throughput screening of gene networ

217 We developed a genome-scale library of ATFs that display an engineered interaction domain (ID)

218 n 48-hour-cultured neurons without effect on ATF-3 expression in Schwann cell nuclei.

219 lase-activating polypeptide had no effect on ATF-3 induction in the 48-hour-cultured cardiac neurons.

220 osmotic stress-induced activation of Plk3 on ATF-2 transcription factor function was also examined in

221 HP also required IRE-1 but not XBP-1 or ATF-6; instead, GCN-2, which is known to suppress transl

222 of nuclear Egr-1 protein and phosphorylated ATF-2.

223 rther downstream, active Plk3 phosphorylated ATF-2 at the Thr-71 site in vivo and in vitro.

224 the AP-1 complex by directly phosphorylating ATF-2 independent from the effects of JNK and p38 activa

225 nner, with JNK-2 being upstream of PKCdelta, ATF-2, and NFkappaB.

226 deletion and point mutation of the predicted ATF/C/EBP binding site in ATF3 promoter abolished lucife

227 This resulted in the accumulation of pro-ATF-6 in the disrupted ER/Golgi membrane network, where

228 CREB (cAMP-response element-binding protein)/ATF family transcription factors, we tested the effect o

229 ivates cAMP response element binding protein/ATF transcription factors, the sterol regulatory element

230 ne of the major ER stress response proteins, ATF-6, and subsequent apoptosis by alterations of CerS6/

231 regulation through its binding to a putative ATF/CRE composite site within the PCK2 promoter function

232 nase (MAPK) activation, resulting in reduced ATF-2 phosphorylation and transcriptional activity.

233 we show that polyamines negatively regulate ATF-2 expression posttranscriptionally and that polyamin

234 tion; specifically, they neither up-regulate ATF-4 and ATF-4 targets nor suppress protein translation

235 ines by ectopic ODC overexpression repressed ATF-2 expression.

236 Moreover, the new class of RHH ATFs may be utilized to re-engineer transcriptional circ

237 ted signal transduction that leads to robust ATF-1/CREB serine 63/133 phosphorylation is not sufficie

238 5 induce degradation of the ER stress sensor ATF-6, leading to activation of the NLRP-3 inflammasome

239 Using reverse genetics, we showed ATF-2 to be functionally required for VEGF-A-stimulated

240 ore, we demonstrate the requirement for Sp3, ATF-2, and p38 for the transcription and protein express

241 ally and that polyamine depletion stabilizes ATF-2 mRNA by enhancing the interaction of the 3'-untran

242 t levels, and neurturin partially suppressed ATF-3 transcript levels in 48-hour cultures.

243 Neurturin significantly suppressed ATF-3 expression in 48-hour-cultured neurons without eff

244 TGFbeta-activated kinase 1 (TAK1)/ATF-2 signaling was disrupted in Smad3(-/-) mouse chondr

245 Loss of Smad3 abrogates TAK1/ATF-2 signaling, most likely by disrupting the Smad3-pho

246 s and secretion of IL-1beta, indicating that ATF-6 is crucial for the induction of this type of cell

247 th anti-acetyl-lysine antibody revealed that ATF-2 can undergo reversible acetylation in vivo.

248 These results show that ATF-1 mediates HO-1 induction by heme and drives macroph

249 Furthermore, we show that ATF-4 is required for PDGF-BB-inducible SMC migration in

250 Moreover, we showed that ATF-2 b-ZIP could serve as an acetyltransferase substrat

251 These results suggest that ATF-2 and SMAD-3 are transcription factors, which are, i

252 eta-oxidation intermediates, suggesting that ATF parasites can use fatty acids as an external carbon

253 The ATF estimated central BP with greater accuracy than GTFs

254 The ATF may permit more accurate, non-invasive central BP mo

255 The ATF was assessed using the original data that helped pop

256 The dimer formed by the ATF-2 and c-Jun transcription factors is one of the main

257 pression differences; genes repressed by the ATF-SKD have stronger binding sites and are more enriche

258 the transcriptional repression caused by the ATF-SKD is not due to changes in active histone modifica

259 We show that Set1 is recruited by the ATF/CREB homolog Atf1 to heterochromatic loci and promot

260 In this study, we have examined the ATF-2 b-ZIP interaction with the p300 HAT domain and sho

261 unctionally conserved components include the ATF/CREB-family heterodimer Atf1-Pcr1 and its CRE-like D

262 Moreover, immune pathways involving the ATF-7 and ZIP-2 transcription factors, which protect C.

263 Transduction of the ATF in MOVCAR 5009 cells derived from ascitic cultures o

264 duced silencing of ATF-2, or mutation of the ATF-2 binding motif prevented the activation of MLCK pro

265 ot exhibit cooperativity with binding of the ATF-2/c-Jun bZIP (leucine zipper dimer with basic DNA re

266 The effect of salt on the formation of the ATF-2/c-Jun dimer and on its ability to bind the target

267 d ER stress response with degradation of the ATF-6 sensor.

268 mediate the anti-metastatic phenotype of the ATF.

269 scription factor 5 (ATF5) is a member of the ATF/cAMP response element-binding family of transcriptio

270 human CHAC1 promoter in the proximity of the ATF/CRE and ACM using ChIP.

271 actor-2 (ATF-2) mRNA encodes a member of the ATF/CRE-binding protein family of transcription factors

272 scription factor 3 (ATF3) is a member of the ATF/CREB subfamily of the basic region-leucine zipper fa

273 anscription factor 3 (ATF3), a member of the ATF/cyclic AMP response element-binding (ATF/CREB) famil

274 scription factor 3 (ATF3) is a member of the ATF/cyclic AMP response element-binding family of transc

275 n levels, whereas HuR silencing rendered the ATF-2 mRNA unstable and prevented increases in ATF-2 mRN

276 epletion did not alter transcription via the ATF-2 gene promoter but increased the stability of ATF-2

277 The ATFs can rapidly induce a single gene driven by a synthe

278 Although the ATFs display widespread binding, few genes showed expres

279 ication of ATF binding sites reveal that the ATFs do not directly target Oct4; instead, they target d

280 , our findings support novel roles for these ATF family members in regulating emotional behavior.

281 ent a quantitative characterization of these ATFs and provide constructs for making their implementat

282 We used this ATF library to screen for key regulators of the pluripot

283 Consistent with this, ATFs were able to utilize exogenous myristate and form b

284 At the 7 day timepoint, ATF-3 signal was significantly smaller in 1 mg MIA treat

285 ting transcription factor-2 (ATF-2) bound to ATF sites in the PTEN promoter.

286 es revealed their potential contributions to ATF-2-mediated transcriptional activation.

287 regulatory proteins Hac1 (for Homologous to ATF/CREB1) and Inositol Requiring Enzyme1 in the plant p

288 ed, except for the proliferative response to ATF.

289 Mutational analysis of the two ATF-2 b-ZIP acetylation sites revealed their potential c

290 omplex with ATF resembles the wild-type uPAR.ATF complex, demonstrating that these mutations do not p

291 y upregulate LAP, downregulate IFN-gamma via ATF-3 expression and acquire a regulatory phenotype.

292 expression at the transcriptional level via ATF-3, which itself was upregulated by 6.9-fold in our c

293 cell nuclei, whereas no neuronal nuclei were ATF-3 immunoreactive.

294 While ATF-2 b-ZIP is a weak inhibitor of hypoacetylated p300 H

295 actor c-Jun and its nuclear association with ATF-2.

296 nuclear compartment and was colocalized with ATF-2 in nuclei.

297 tructure of uPAR(H47C/N259C) in complex with ATF resembles the wild-type uPAR.ATF complex, demonstrat

298 g at 4 hours, the percentage of neurons with ATF-3-immunoreactive nuclei increased progressively, and

299 approaches to DNA recognition compared with ATFs that involve binding of a single protein.

300 The basic leucine zipper ATF-like 3 (BATF3)-dependent CD103(+)CD11b(-) dendritic

301 ination, both migratory basic leucine zipper ATF-like transcription factor 3 (BatF3)-dependent and Ba