ライフサイエンスコーパス: ATF2

1 c-Jun and activating transcription factor 2 (ATF2).

2 tion of an AP1 complex (containing c-Jun and ATF2).

3 phospho-CREB and cytoplasmic accumulation of ATF2.

4 inhibited JNK activity via competition with ATF2.

5 or ATP and noncompetitive inhibition against ATF2.

6 l of the basic region leucine zipper protein ATF2.

7 targets the transcription factors c-Jun and ATF2.

8 ased levels of the histone acetyltransferase ATF2.

9 ncluding the transcription factors c-Jun and ATF2.

10 and requires transcription factors c-Jun and ATF2.

11 phosphorylation of the transcription factor ATF2.

12 y blocked by ATF2DeltaN, a dominant negative ATF2.

13 t binds transcription factors c-Jun and CREB/ATF2.

14 de derived from amino acid (aa) 51 to 100 of ATF2.

15 ion of the AP-1-related transcription factor ATF2.

16 vated protein (MAP) kinase and its substrate ATF2.

17 yclase, ADCY8, and the transcription factor, ATF2.

18 horylation and transcriptional activation of ATF2.

19 , a transcription factor homologous to human ATF2.

20 r63 and Ser73 of c-Jun or Thr69 and Thr71 of ATF2.

21 lates and activates the transcription factor ATF2.

22 IL-23p19 indirectly, likely via reduction of ATF2.

23 y regulates the transcriptional potential of ATF2.

24 effectively influenced protein expression of ATF2.

25 is maintained through the JNK activation of ATF2.

26 ed on the delta-domain sites of JIP ( 3) and ATF2 ( 1) were not recognized by p38, also of the MAPK f

27 Expression of ATF2(150-248) in fibroblasts or melanoma but not in ATF2

28 Constitutive expression of ATF2(150-248) peptide outcompeted TIP49b interaction wit

29 and requires amino acids 150 to 248 of ATF2 (ATF2(150-248)), which are implicated in intramolecular i

30 able of processing natural protein substrate ATF2; 172 site phosphorylation did not.

31 Phosphoantibodies to ATF2(490/8) reveal dose- and time-dependent phosphorylat

32 Furthermore, ATF2(50-100) binds to c-Jun N-terminal kinase (JNK) and

33 Here we demonstrate that ATF2(50-100) induced apoptosis by sequestering ATF2 to t

34 Mutations within the JNK binding region of ATF2(50-100) or expression of TAM67 or JunD RNAi attenua

35 Mutation within ATF2(50-100) that impairs association with JNK and the i

36 s sensitization of melanoma cells expressing ATF2(50-100) to apoptosis after treatment with anisomyci

37 and B16F10 mouse melanomas were inhibited by ATF2(50-100) to varying degrees up to a complete regress

38 peptide spanning amino acids 50-100 of ATF2 (ATF2(50-100)) reduces ATF2 transcriptional activities wh

39 ived from activating transcription factor 2 (ATF2(50-100)).

40 NA interference (RNAi) reduces the degree of ATF2(50-100)-induced apoptosis.

41 s inhibition of melanoma's tumorigenicity by ATF2(50-100).

42 ed (+/-250 bp) with RUNX3 (64%), BATF (55%), ATF2 (51%), IRF4 (41%), MEF2A (35%), PAX5 (34%), SPI1 (2

43 Here we show that expression of ATF2((51-100)) in human melanoma cells reduced their gro

44 In addition, loss of ATF2/7 desensitises Emu-Myc lymphoma cells to spontaneou

45 Despite the delayed p38MAPK activation, ATF2, a substrate of p38MAPK, is still phosphorylated, l

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

47 Targeted mutation of ATF2 abrogates both constitutive and inducible expressio

48 Formation of c-JUN-ATF2-activated heterodimers was increased after AA limit

49 Transcription factors ATF2 (activating transcription factor 2) and ATF7 (activ

50 splenic tumors, controlled the expression of ATF2 (activating transcription factor 2).

51 Reduced or heightened ATF2 activity also sensitizes or desensitizes cells to E

52 nt with this concept, the phosphorylation of ATF2 along with the expression and phosphorylation of c-

53 se in transcriptional activity by endogenous ATF2 and a markedly increased sensitivity to the four ag

54 peptide outcompeted TIP49b interaction with ATF2 and alleviated the suppression of ATF2 transcriptio

55 c-MYC induces stress-mediated activation of ATF2 and ATF7 and that these transcription factors regul

56 The B cell-specific deletion of ATF2 and ATF7 in mice results in significantly accelerat

57 ism for JNK1beta1 with transcription factors ATF2 and c-Jun along with interaction kinetics for these

58 ATF2 and c-Jun are key components of activating protein-

59 Both ATF2 and c-Jun interact with a novel enhancer in the int

60 Together, these findings demonstrate that ATF2 and c-Jun mutually regulate each other by altering

61 immunoprecipitation with antibodies against ATF2 and c-Jun or their phosphorylated forms and hybridi

62 K(m) for ATF2 and c-Jun was 1.1 and 2.8 muM, respectively.

63 nse occurs at least partly via activation of ATF2 and c-Jun, leading to large-scale coordinate gene e

64 e affinity of unphosphorylated JNK1beta1 for ATF2 and c-Jun, to 0.80 +/- 0.04 versus 0.65 +/- 0.07 mu

65 rgistically activated promoter activity with ATF2 and c-Jun.

66 The induction is mediated by ATF2 and c-Jun.

67 and activation of AP-1 components including ATF2 and c-Jun.

68 promoters are bound upon phosphorylation of ATF2 and c-Jun.

69 ibited pure noncompetitive inhibition versus ATF2 and competitive inhibition versus ATP.

70 ssion of the downstream transcription factor ATF2 and completely blocked by ATF2DeltaN, a dominant ne

71 on leads to the decreased phosphorylation of ATF2 and consequent increased expression of the melanocy

72 or-activated receptor-gamma accompanied with ATF2 and CREB (cAMP-response element-binding protein) wa

73 e and activate the two transcription factors ATF2 and Elk-1.

74 Moreover, shRNA silencing of ATF2 and FoxP3 reveals an important role of ATF2-FoxP3 p

75 Significantly, a reduction of nuclear ATF2 and increased beta-catenin expression were seen in

76 Conversely, cytosolic ATF2 and induction of IFNbeta1 coincides with therapeuti

77 c-Jun in the nucleus prevents the export of ATF2 and is essential for the transcriptional activation

78 symmetrically located amino acid residues in ATF2 and Jun facilitated the interactions between hetero

79 Different regions of ATF2 and Jun mediated their orientation-dependent transc

80 Notably, nuclear ATF2 and low expression of IFNbeta1 in melanoma tumor sa

81 on and Mkk4(-/-) ESCs exhibited diminished p-ATF2 and MEF2C expression, resulting in impaired MHC ind

82 creased expression of c-JUN was dependent on ATF2 and on activation of the MEK-ERK and JNK arms of th

83 perturbation resulted in the accumulation of ATF2 and RNF20 and the promiscuous accumulation of DDR-a

84 A and protein expression of c-Fos, c-Jun and ATF2 and sustained repression of Fra-2.

85 ctly upregulating gene expression (c-fos and ATF2) and by activating pathways that stimulate AP-1 act

86 oteins (c-Jun dimerization protein 2 [JDP2], ATF2, and histone deacetylase 6 [HDAC6]), as determined

87 d elevated phosphorylation of MKK4, p38, and ATF2, and increased MEF2C expression.

88 tion of interferon response factor 3 (IRF3), ATF2, and NF-kappaBp65.

89 causes activation of calcineurin (Cn), NFAT, ATF2, and NFkappaB/Rel factors, which collectively alter

90 hat cAMP acts through the PKA/CREB, PKA/PI3K/ATF2, and PKA/ERK/ATF2 pathways to control a key vascula

91 Thus, c-Jun, ATF2, and TCFs are required to connect the intracellular

92 F2DeltaN), increases activities of p38 MAPK, ATF2, and the level of TNFalpha expression.

93 cells by activating transcription of c-Jun-, ATF2-, and TCF-controlled genes.

94 Although it has been believed that c-Jun and ATF2 are constitutively localized in the nucleus, where

95 ansport (e.g. QDR2, YBT1), lipid metabolism (ATF2, ARE1), cell stress (HSP12, CTA1), DNA repair (YIM1

96 -driven mouse B-cell lymphomas, we find that ATF2 as well as MAP kinase c-Jun N-terminal kinase (JNK)

97 ATF2 association with TIP60 on chromatin is decreased fo

98 ed ATF2 phosphorylation and increased TIP49b-ATF2 association.

99 ndent and requires amino acids 150 to 248 of ATF2 (ATF2(150-248)), which are implicated in intramolec

100 of a peptide spanning amino acids 50-100 of ATF2 (ATF2(50-100)) reduces ATF2 transcriptional activit

101 We demonstrate here that ATF2, ATF3, and ATF4 are each robustly induced in the nu

102 Because amphetamine and stress induce ATF2, ATF3, and ATF4 in nucleus accumbens, and overexpre

103 siRNA-based depletion of c-Jun and ATF2 attenuated TNFalpha action on Map4k4 mRNA expressio

104 Activating transcription factor 2 (ATF2) belongs to the basic leucine zipper family of tran

105 d kinase inhibitors down-regulated Thr(P)-71-ATF2 binding to the il23a promoter and il23a mRNA expres

106 K, and p38 MAPK inhibitors blunted Thr(P)-69-ATF2 binding.

107 Thr(P)-69-activating transcription factor 2 (ATF2) binding in response to zymosan.

108 fied this region as a core sequence to which ATF2 binds.

109 Similarly, ATF2 bound to opposite half-sites in Fos-ATF2-NFAT1 and

110 l mobility shift assays revealed that mainly ATF2 bound to this CRE-like element, and mutation of the

111 dose- and time-dependent phosphorylation of ATF2 by ATM that results in its rapid colocalization wit

112 rylations on N-terminal Thr-71 and Thr-69 of ATF2 by ERK and p38 MAPK, MEK, and p38 MAPK inhibitors b

113 ivation of nuclear factor-kappaB, c-jun, and ATF2 by TNF was comparable in HUAECs and HUVECs, whereas

114 ylated rapidly and this methylation inhibits ATF2/c-Jun and CREB transcription factor binding in vitr

115 that may mediate a repressor effect because ATF2 can heterodimerize with other bZIP molecules.

116 Jun dimerization with Fos versus ATF2 caused it to bind opposite half-sites at nonconsens

117 tions detected included HBZ with MAFB, MAFG, ATF2, CEBPG, and CREBZF and MEQ with NFIL3.

118 in the presence and absence of both ATP and ATF2 competitive inhibitors.

119 t or -deficient cells and requires the Smad1-Atf2 complex that facilitates their recruitment to the p

120 Activating transcription factor 2 (ATF2/CRE-BP1) is implicated in transcriptional control o

121 like the yeast GCN4, and the mammalian JUN, ATF2, CREB, C/EBP, and PAR leucine zippers, characterize

122 that control mitochondrial function, such as ATF2, CREB, PGC1alpha, DIO2, NRF1, CYTC, COX2, ATP5beta,

123 , as well as transcription factors including Atf2, Creb3l1, and Erg.

124 One of these clones, termed ATF2 deletion (ATF2d), encodes a novel ATF2 isoform and

125 creased cellular survival and revealed c-Jun/ATF2-dependent control of ATF3 expression.

126 insight into regulation of ATM activation by ATF2-dependent control of TIP60 stability and activity.

127 st explained through coordinated kappaB- and ATF2-dependent transcription; and (iii) il23a expression

128 ), and strongly increase phosphorylation and ATF2-dependent transcriptional activity.

129 ific combinations of c-Jun, CREB1, ATF1, and ATF2 dimers.

130 ly, stable expression of a dominant negative ATF2 (dnATF2) quantitatively blocks phosphorylation of e

131 The transcription factor ATF2 elicits oncogenic activities in melanoma and tumor

132 The p38/JNK-ATF2/Elk-1bifan synchronizes the output of activated tra

133 toxic stress attenuates PKCepsilon effect on ATF2; enables ATF2 nuclear export and localization at th

134 Moreover, the wild type ATF2-expressing clones exhibited rapid DNA repair after

135 Importantly, inhibition of ATF2 expression by small interfering RNA in CD4(+) cells

136 Inhibition of ATF2 expression decreased recruitment of Mre11 to IRIF,

137 anoma, we evaluated the pattern and level of ATF2 expression in a large cohort of melanoma specimens.

138 Inhibition of ATF2 expression in these lines restored TIP60 protein le

139 elanoma and prostate cancer cell lines whose ATF2 expression is inversely correlated with TIP60 level

140 The clinical significance of ATF2 expression is unknown.

141 Strong nuclear ATF2 expression was associated with metastatic specimens

142 Strong cytoplasmic ATF2 expression was associated with primary specimens ra

143 However, activating transcription factor-2 (ATF2) expression was significantly lower in CD8(+) compa

144 nt with these findings, keratinocytes of K14.ATF2(f/f) mice exhibit greater anchorage-independent gro

145 Papillomas of K14.ATF2(f/f) mice exhibit reduced expression of presenilin1

146 2-tetradecanoate 13-acetate (DMBA/TPA)], K14.ATF2(f/f) mice showed significant increases in both the

147 expressed ATF2 mutant with K14-Cre mice (K14.ATF2(f/f)) resulted in selective expression of mutant AT

148 2 were poor substrates relative to c-Jun and ATF2 for active recombinant JNK1.

149 duced p19 promoter activation, and c-Jun and ATF2 formed a protein complex, demonstrated by co-immuno

150 ATF2 and FoxP3 reveals an important role of ATF2-FoxP3 pathway in the anisomycin-induced apoptosis o

151 CREB) and activating transcription factor 2 (ATF2), function as a transcriptional activator and a rep

152 sistent with this, both Gal4-c-Jun- and Gal4-ATF2-fusion proteins were activated by RalA signalling t

153 on factor activating transcription factor 2 (ATF2) has been shown to be associated with melanocytic o

154 c-Jun-ATF2 heterodimers activate the expression of many target

155 fibre bundles and that of ERK1/2, RSK1/2 and ATF2 in both fibre types.

156 We conclude that inhibition of ATF2 in concert with increased JNK/Jun and JunD activiti

157 Stable expression of ATF2 in human breast carcinoma BT474 cells increases tra

158 insight into the pathophysiological role of ATF2 in human diseases.

159 = 25 +/- 6 nM) competitive inhibitor versus ATF2 in JNK3alpha1.

160 e CREB or a constitutively nuclear-localized ATF2 in LNCaP cells inhibits IR-induced NE-like differen

161 To determine the prognostic value of ATF2 in melanoma, we evaluated the pattern and level of

162 thereby indicating a suppressor activity of ATF2 in skin tumor formation.

163 Our findings identify a role for ATF2 in the DNA damage response that is uncoupled from i

164 d transformation and reveal a novel role for ATF2 in the inhibition of the Ras-Raf-MEK-ERK signaling

165 nditions, activating transcription factor-2 (ATF2) in cooperation with Cul3 ubiquitin ligase promotes

166 ctions of activating transcription factor-2 (ATF2) in the development and therapeutic resistance of m

167 vealed a positive feedback mechanism whereby ATF2 induces p38 MAPK phosphorylation to further induce

168 O80 chromatin-remodeling complex, as a novel ATF2-interacting protein.

169 in consisting of HIV-TAT and aa 51 to 100 of ATF2 into SW1 melanomas efficiently inhibits their growt

170 We previously demonstrated that ATF2 is a nucleocytoplasmic shuttling protein, and it co

171 Although elevated expression of ATF2 is also required for v-Rel-mediated transformation,

172 ATF2 is among transcription factors implicated in the pr

173 The transcription potential of ATF2 is enhanced markedly by NH2-terminal phosphorylatio

174 l findings in which transcriptionally active ATF2 is involved in tumor progression-proliferation in m

175 Nuclear ATF2 is likely to be transcriptionally active, whereas c

176 TIP49b's association with ATF2 is phosphorylation dependent and requires amino aci

177 Activation of Jun and ATF2 is severely diminished in Bmp7-null kidneys, provid

178 The activating transcription factor 2 (ATF2) is a member of the ATF/cAMP-response element-bindi

179 Activating transcription factor 2 (ATF2) is regulated by JNK/p38 in response to stress.

180 ermed ATF2 deletion (ATF2d), encodes a novel ATF2 isoform and was chosen for further characterization

181 n proposed to require a fixed orientation of ATF2-Jun binding.

182 Our results show that ATF2-Jun heterodimers bound IFNb in both orientations al

183 ATF2-Jun heterodimers that bound IFNb in opposite orient

184 FNb in association with both orientations of ATF2-Jun heterodimers with the same cooperativity.

185 ATF2-Jun, IRF3, and HMGI recognize a composite regulator

186 Cooperative ATF2-Jun-IRF3 complex formation at IFNb has been propose

187 to opposite half-sites in Fos-ATF2-NFAT1 and ATF2-Jun-NFAT1 complexes.

188 increased after AA limitation, and c-JUN or ATF2 knockdown suppressed the induction of c-JUN and oth

189 ATF2d retains the bZIP domain of ATF2, lacks the N-terminal zinc-finger region, and inclu

190 atively blocks phosphorylation of endogenous ATF2 leading to a marked decrease in transcriptional act

191 TGFbeta enhanced the activation of ATF2, leading to increased phospho-ATF2 levels within th

192 vation of ATF2, leading to increased phospho-ATF2 levels within the DNA-protein complexes.

193 t transcription required the presence of the ATF2-like AP1-site at -70 bp and the c-Jun binding motif

194 eletion causes a frame shift, resulting in a ATF2-like polypeptide of approximately 60 kDa.

195 A favorable prognosis was predicted by ATF2 ln(non-nuclear/nuclear AQUA score ratio) of more th

196 ere is a sub-population of Her2(+)p-p38(lo)p-Atf2(lo)Twist1(hi)E-cad(lo) early cancer cells that is i

197 ein kinase C-varepsilon (PKCvarepsilon)- and ATF2-mediated mechanism that facilitates resistance by t

198 f PKCvarepsilon with chemotherapies relieves ATF2-mediated transcriptional repression of IFNbeta1, re

199 f papilloma development compared with the WT ATF2 mice.

200 Moreover, our findings suggest that ATF2 might be a useful prognostic marker in early-stage

201 Knockdown of atf2 mRNA with siRNA correlated with inhibition of il23a

202 Relative to ATF2 mRNA, this clone contains an internal 97-nt deletio

203 In addition, a phosphorylation-negative ATF2 mutant construct decreased basal and TGFbeta-mediat

204 Crossing the conditionally expressed ATF2 mutant with K14-Cre mice (K14.ATF2(f/f)) resulted i

205 ors, JUN, activating transcription factor 2 (ATF2), myocyte-specific enhancer factor 2A (MEF2A), and

206 ly, ATF2 bound to opposite half-sites in Fos-ATF2-NFAT1 and ATF2-Jun-NFAT1 complexes.

207 eighbored genes associated with SCZ (NOS1AP, ATF2, NSF, and PIK3C3).

208 PKCepsilon, as seen in melanoma cells, block ATF2 nuclear export and function at the mitochondria, th

209 ttenuates PKCepsilon effect on ATF2; enables ATF2 nuclear export and localization at the mitochondria

210 a is determined by PKCepsilon, which directs ATF2 nuclear localization.

211 0-248) in fibroblasts or melanoma but not in ATF2-null cells caused a profound G(2)M arrest and incre

212 Although analysis of Atf2-null NK cells shows no defect, the transgenic mice

213 tly, c-Jun-dependent nuclear localization of ATF2 occurs during retinoic acid-induced differentiation

214 the p38alpha transcription factor substrate ATF2 occurs in a precise sequence.

215 e that the protein kinase ATM phosphorylates ATF2 on serines 490 and 498 following ionizing radiation

216 n relies on complementary phosphorylation of ATF2 on Thr-69 and Thr-71 dependent on PKC and MAPK acti

217 tanding how subcellular localization enables ATF2 oncogenic or tumor suppressor functions.

218 Inhibiting either ATF2 or Cul3 expression by small interfering RNA stabili

219 expression of a dominant-negative mutant of ATF2 or expression of an ATF2-specific short hairpin RNA

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

221 ot alter the expression of CREB, CREM, ATF1, ATF2, or ATF4 proteins.

222 l activation through c-Jun but not the ATF1, ATF2, or CREB transcription factor.

223 hese results, overexpression of c-Jun, ATF1, ATF2, or CREB1 in transiently transfected osteoblastic c

224 nhibition, whereas transfection of Creb1 and Atf2 overexpression constructs enhanced cAMP-driven Cd39

225 g viral-mediated gene transfer, we show that ATF2 overexpression in nucleus accumbens produces increa

226 ympathetic stimulation through the cAMP-CREB/ATF2 pathway.

227 morphogenetic protein-Smad1 and Atm-p38MAPK-Atf2 pathways in p53-proficient or -deficient cells and

228 ugh the PKA/CREB, PKA/PI3K/ATF2, and PKA/ERK/ATF2 pathways to control a key vascular homeostatic medi

229 mechanisms underlying the activities of the ATF2 peptide while highlighting its possible use in drug

230 Peptide inhibitors from both ATF2 (peptide 1) and JNK-interacting protein 1 (JIP-1) (

231 rom the phosphoacceptor activation domain on ATF2 (peptides 4 and 5) were recognized neither as subst

232 he first time in VSMC that TGFbeta activates ATF2 phosphorylation and Csrp2 gene expression via a CRE

233 tivation of p38 kinase, all of which induced ATF2 phosphorylation and increased TIP49b-ATF2 associati

234 TA treatment resulted in an increase in ATF2 phosphorylation, which was followed by a subsequent

235 equential nature of the JNK2alpha2 catalyzed ATF2 phosphorylation.

236 c-Jun and activating transcription factor-2 (ATF2) phosphorylation and binding to the PI.3/PII region

237 dicate that JNK-dependent phosphorylation of ATF2 plays an important role in the drug resistance phen

238 Here we show that ATF2 possesses a nuclear export signal in its leucine zi

239 ranscriptionally active, whereas cytoplasmic ATF2 probably represents an inactive form.

240 factor IRF3, and activator of transcription ATF2, reaching levels similar to those seen in C(ko) vir

241 ATF2 regulates target gene expression by binding to the

242 Activating transcription factor 2 (ATF2) regulates transcription in response to stress and

243 Investigating the mode of ATF2 regulation revealed a positive feedback mechanism w

244 resistance of melanoma via the PKCvarepsilon-ATF2 regulatory axis.

245 The activation of the JNK-ATF2 reporter was mediated by the DEP domain of Dishevel

246 lts suggest that cytoplasmic localization of ATF2 requires function of at least one of the NESs.

247 ATF2 requires neither JNK/p38 nor its DNA binding domain

248 Overexpression of ATF2 resulted in significant increase in ATF3 promoter a

249 H(2)-terminal kinase with c-Jun but not with ATF2, resulting in concomitant increase in TRE-mediated

250 a peptide that corresponds to aa 51 to 60 of ATF2 sensitizes melanoma cells to spontaneous apoptosis,

251 led the induction was mediated by a p38-MAPK-ATF2 signaling pathway and that RNAi-mediated inhibition

252 Elevated Mapk14-Atf2 signaling predicted poor response to sorafenib ther

253 g Mapk14-dependent activation of Mek-Erk and Atf2 signaling.

254 -negative mutant of ATF2 or expression of an ATF2-specific short hairpin RNA interfered with TRPM3-me

255 had both weak cytoplasmic and strong nuclear ATF2 staining had the worst outcome, both among the full

256 their transcription factor effectors (c-Jun, ATF2, Stat3 and NF-kappaB) affects TNF, Fas and TRAIL re

257 Thus, ATF2 subcellular localization is probably modulated by m

258 cancer cells, suggesting that alteration of ATF2 subcellular localization may be involved in the pat

259 d further understanding of the regulation of ATF2 subcellular localization under various pathological

260 ntial kinetic mechanism and that the ATP and ATF2 substrate sites were non-interacting.

261 sphorylation by MKK6, kinase activity toward ATF2 substrate, thermal stability, and X-ray crystal str

262 ir transcription factor substrates c-Jun and ATF2, suggesting that D-site-containing substrates also

263 NES enhances the transcriptional activity of ATF2, suggesting that the novel NES negatively regulates

264 d JNK2-mediated phosphorylation of c-Jun and ATF2, suggesting that transcription factors, MKK4, and t

265 Furthermore, co-transfection of c-Jun and ATF2 synergistically induced p19 promoter activation, an

266 Inhibition of ATF2 target gene expression via expression of a dominant

267 is associated with transgenic insertion into Atf2, the gene for the basic leucine zipper (bZIP) trans

268 the phosphorylation of CREB1 (Ser(133)) and ATF2 (Thr(71)) in a PKA-, PI3K-, and ERK-dependent fashi

269 of CREB, transcription factor 1 (ATF1), and ATF2, three transcription factors that bind to the cycli

270 a shift in the K(D) of the active kinase for ATF2 to 1.70 +/- 0.25 muM and for c-Jun of 3.50 +/- 0.95

271 ta1 decreased the affinity of the kinase for ATF2 to 11.0 +/- 1.1 muM and for c-Jun to 17.0 +/- 7.5 m

272 ted that binding of phosphorylated CREB1 and ATF2 to cAMP-response element-like sites was significant

273 The ability of ATF2 to reach the mitochondria is determined by PKCepsil

274 F2(50-100) induced apoptosis by sequestering ATF2 to the cytoplasm, thereby inhibiting its transcript

275 f the c-JUN gene by recruitment of c-JUN and ATF2 to two AP-1 sites within the proximal promoter.

276 g through activating transcription factor 2 (ATF2) to the cyclic adenosine monophosphate (AMP) respon

277 Furthermore, ATF2-transactivated Csrp2 promoter activity and TGFbeta

278 Finally, we identified a putative Atf2 transcription factor, which is required for APP1 tr

279 tors resulting in phosphorylation of Jun and ATF2 transcription factors.

280 Altering the balance of Jun/ATF2 transcriptional activities sensitized melanoma cell

281 expression of TIP49b efficiently attenuated ATF2 transcriptional activities under normal growth cond

282 acids 50-100 of ATF2 (ATF2(50-100)) reduces ATF2 transcriptional activities while increasing the exp

283 e implicated in intramolecular inhibition of ATF2 transcriptional activities.

284 with ATF2 and alleviated the suppression of ATF2 transcriptional activities.

285 Our data reveal that loss of ATF2 transcriptional activity serves to promote skin tum

286 e transgenic mice express abnormal truncated Atf2 transcripts that may mediate a repressor effect bec

287 Here, we identify that ATF2 tumor suppressor function is determined by its abil

288 c-jun and activating transcription factor 2 (ATF2) upon activation by a variety of stress-based stimu

289 Inhibition of ATF2 via RNA interference likewise increased c-Jun expre

290 Cytoplasmic localization of ATF2 was observed in melanoma, brain tissue from patient

291 Here, we use a mouse model in which ATF2 was selectively deleted in keratinocytes.

292 ATF2 was significantly increased in the same group.

293 tes JNK, which then phosphorylates c-Jun and ATF2 when bound to the c-jun promoter.

294 ite in the dp5 promoter that binds c-Jun and ATF2, which is critical for dp5 promoter induction after

295 ways are mediated through phosphorylation of ATF2, which is mediated by p38 MAPK-, JNK- and ERK-depen

296 ha1 activity in a competitive fashion versus ATF2 while being pure noncompetitive toward ATP.

297 wed that unphosphorylated JNK1beta1 bound to ATF2 with similar affinity as it did to c-Jun (K(D) = 2.

298 f JNK-dependent transcription factors (c-Jun/ATF2) with activated IRF3 in the induction of primary IR

299 ) resulted in selective expression of mutant ATF2 within the basal layer of the epidermis.

300 r anchorage-independent growth compared with ATF2 WT keratinocytes.