ライフサイエンスコーパス: ATF6

1 R) sensor activating transcription factor 6 (ATF6).

2 PERK) and activating transcription factor 6 (ATF6).

3 ctor, activated transcription factor 6alpha (ATF6).

4 cation of activating transcription factor 6 (ATF6).

5 including activating transcription factor 6 (ATF6).

6 vates the activating transcription factor 6 (ATF6).

7 nfirms accumulation of precursor SREBP-1 and ATF6.

8 protection was reversed by dominant-negative ATF6.

9 ta cell proliferation, through activation of ATF6.

10 d the ER stress response regulators XBP1 and ATF6.

11 of activating transcription factors ATF4 and ATF6.

12 APK) pathway for controlling the activity of ATF6.

13 major immediate-early promoter by XBP1s and ATF6.

14 silencing the UPR transducers IRE-1alpha and ATF6.

15 s affected by the inhibition of IRE1alpha or ATF6.

16 F6f, the transcriptional activator domain of ATF6.

17 intramembrane proteolysis and activation of ATF6.

18 s in ATF4, CHOP10, and XBP1s and cleavage of ATF6.

19 way markers Xbp1, PERK, eIF2alpha, Hspa5 and ATF6.

20 egrity of the ER and Golgi and processing of ATF6.

21 eavage of the mammalian transcription factor ATF6.

22 t with the ER-localized transcription factor ATF6.

23 sses a novel conditionally activated form of ATF6.

24 and activation of the transcription factor, ATF6.

25 rough the activation of PERK, IRE1/XBP1, and ATF6.

26 ponses through the effectors, PERK, IRE1 and ATF6.

27 eased expression of the transcription factor ATF6.

28 ) branch of the UPR by expression of spliced ATF6(1-373) decreased intracellular accumulation of ATZ

29 Expression of ATF6(1-373) did not cause inhibition of protein synthesi

30 Expression of ATF6(1-373) in ATZ-expressing hepatoma cells did not ind

31 Here, we analyzed ATF6, a type II transmembrane glycoprotein that serves a

32 the ER, activating the transcription factor, ATF6 (activating transcription factor 6 alpha), which in

33 entiation primary response gene 88), but not ATF6 (activating transcription factor 6) or XBP1 (X-box-

34 rom iPLA2gamma knock-out mice showed blunted ATF6 activation and chaperone up-regulation in response

35 In this mouse line, ATF6 activation decreased ischemic damage in an ex vivo

36 s interrupt distinct sequential steps of the ATF6 activation mechanism.

37 r molecules phenocopy the ability of genetic ATF6 activation to selectively reduce secretion and extr

38 We found that IRE1 and ATF6 activities were attenuated by persistent ER stress

39 6S) appears to be a more potent inhibitor of ATF6 activity.

40 Thus, the relative levels of ATF6 alpha and -beta, may contribute to regulating the s

41 N-ATF6 alpha and N-ATF6 beta translocate to the nucleus, b

42 beta inhibited the binding of recombinant N-ATF6 alpha to an ERSR element from the GRP78 promoter.

43 ed loss-of-function and high expression to N-ATF6 alpha, suggesting that ATF6 beta is an endogenous i

44 that ATF6 beta is an endogenous inhibitor of ATF6 alpha.

45 dependent activation of XBP1s, or especially ATF6, also attenuates extracellular aggregation of amylo

46 A transcription factor complex consisting of ATF6 (an endoplasmic reticulum-resident factor) and C/EB

47 activated activating transcription factor 6 (ATF6), an unfolded protein response (UPR) pathway transc

48 ion factor 6 alpha (ATF6alpha, also known as ATF6)--an integral branch of the unfolded protein respon

49 Recently, we have identified that ATF6, an endoplasmic reticulum-resident transcription fa

50 Here, we show that ATF6, an ER stress-induced transcription factor, interac

51 wever, with long-term pressure overload both Atf6 and Atf6b null mice showed enhanced decompensation

52 ATF6 and BBF2H7 are transmembrane basic leucine zipper t

53 rogramming of the UPR seen at both the mRNA (Atf6 and Bip) and protein (pATF6 and peIf2alpha) levels,

54 IFN-stimulated proteolytic processing of ATF6 and ERK1/2-mediated phosphorylation of C/EBP-beta a

55 Unexpectedly, degradation of endogenous ATF6 and exogenously expressed chicken and human ATF6 by

56 ow CerS6/C(16)-ceramide alteration activates ATF6 and induces ER-stress-mediated apoptosis in squamou

57 It also increased the level of ATF6 and intracellular localization into the nuclei in t

58 ranslational response arm, together with the ATF6 and IRE1-XBP1-mediated transcriptional arms, have b

59 The ATF6 and IRE1/XBP1 pathways are separate ER stress-respo

60 ntinued activation of cell survival factors, Atf6 and Ire1alpha during chronic ER stress due to prese

61 lational control, but also for activation of ATF6 and its target genes.

62 ases 1/2 (ERK1/2) promotes the expression of ATF6 and leads to further increase of myocardin transcri

63 molecules requires activation of endogenous ATF6 and occurs independent of global ER stress.

64 However, both ATF6 and PERK branches of the UPR(ER) participate in ame

65 The aim of this study was to investigate how ATF6 and PERK signaling affected misfolded rhodopsin in

66 ion of ER stress-associated proteins (GRP78, ATF6 and PERK) and correlated with clinical outcome in E

67 IFN-gamma-induced proteolytic processing of ATF6 and phosphorylation of C/EBP-beta are obligatory fo

68 IFN-gamma-induced proteolytic processing of ATF6 and phosphorylation of C/EBP-beta were essential fo

69 ulates ESC-SMC differentiation by activating ATF6 and promoting myocardin expression.

70 ed intramembrane proteolysis (RIP) of OASIS, ATF6 and SREBP transcription factors, consistent with de

71 R stress to explore the relationship between Atf6 and steatosis.

72 cluding the unfolded protein response sensor ATF6 and the ER degradation cluster that included FAF1,

73 Activation of ATF6 and the GRP78 promoter, as well as grp78 mRNA accum

74 ction by other ER stresses was found to bind ATF6 and to be critical for maximal ischemia-mediated GR

75 RK pathway facilitates both the synthesis of ATF6 and trafficking of ATF6 from the ER to the Golgi fo

76 Comparing the time course of induction of ATF6 and XBP1 targets suggested that the two pathways ha

77 he unfolded protein response proteins GRP78, ATF6 and XBP1s were found expressed in CP and PDAC perit

78 ate autophagy in CLL patient samples lacking ATF6 and/or C/EBP-beta.

79 ticulum stress sensors (IRE1alpha, PERK, and ATF6) and allows them to activate the apoptotic signalin

80 inducing activating transcription factor-6 (ATF6) and C/EBP homology protein (CHOP).

81 vation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regula

82 Activating transcription factor 6 (ATF6) and protein kinase RNA-like endoplasmic reticulum

83 1 (IRE1), activated transcription factor 6 (ATF6) and their downstream targets glucose-regulated pro

84 in 1, and activating transcription factor 6 (ATF6), and each of these pathways has been implicated to

85 R stress (increased phospho-eIF2alpha, KDEL, ATF6, and CHOP).

86 ads to accumulation of precursor SREBP-1 and ATF6, and development of insufficient reserves of their

87 e (UPR), activated by sensor molecules PERK, ATF6, and IRE1 to resolve endoplasmic reticulum (ER) str

88 Three ER stress sensors (PERK, ATF6, and IRE1) implement the UPR.

89 es in the lens exhibited activation of IRE1, ATF6, and PERK associated with expansion of the endoplas

90 served the fundamental UPR transducers IRE1, ATF6, and PERK.

91 downstream of the ER membrane proteins IRE1, ATF6, and PERK.

92 of the unfolded protein response, IRE1alpha, ATF6, and PKR-like eIF2alpha kinase (PERK), significantl

93 g branches initiated by IRE1alpha, PERK, and ATF6 are crucial for tumor growth and aggressiveness as

94 at selective pharmacologic activation of the ATF6 arm of the unfolded protein response (UPR) during r

95 e for the activating transcription factor 6 (ATF6) arm of the UPR in mitigating adverse outcomes asso

96 The IRE1alpha/ATF6 arms of the UPR offer a potential therapeutic targe

97 a novel interplay between PERK and the XBP1-ATF6 arms of the UPR, whereby PERK attenuates the expres

98 alpha and activating transcription factor 6 (ATF6) arms of the UPR compared with untreated cells.

99 This suggests ATF6 as a potential therapeutic target for intervening i

100 ngs reveal a redundant function of XBP1s and ATF6 as activators of the viral life cycle, and an unexp

101 dentified activating transcription factor 6 (ATF6) as a genetic cause of achromatopsia.

102 ice exhibited increased expression of Grp78, ATF6, ATF4, and spliced XBP1 in CD8alphabeta(+) IEL but

103 Cardiac myocyte-specific deletion of Atf6 (ATF6 cKO [conditional knockout]) blunted transvers

104 utyric acid, or adenoviral transfection with ATF6 attenuated HNE-induced monocyte adhesion and IL-8 i

105 sponse (UPR)-associated transcription factor ATF6 attenuates secretion and extracellular aggregation

106 N-ATF6 beta conferred loss-of-function and high expression

107 inding experiments showed that recombinant N-ATF6 beta inhibited the binding of recombinant N-ATF6 al

108 expression to N-ATF6 alpha, suggesting that ATF6 beta is an endogenous inhibitor of ATF6 alpha.

109 N-ATF6 alpha and N-ATF6 beta translocate to the nucleus, bind to specific r

110 cterial defense, but also expand the role of ATF6 beyond ER stress.

111 ATF6 binds to ER stress response elements in target gene

112 phosphorylated, but the amounts of Ig kappa, ATF6, BiP, Cyclin B2, OcaB (BOB1, Pou2af1), and XBP1 mRN

113 In the in vitro reaction, the ATF6-BiP complex disassembles when membranes are treated

114 on of the activating transcription factor 6 (ATF6) branch of the UPR by expression of spliced ATF6(1-

115 rotein response pathway transcription factor ATF6 (but not Ire1 or PERK).

116 and exogenously expressed chicken and human ATF6 by the proteasome required SEL1L.

117 d all three ER stress pathways (PERK, IRE1a, ATF6) by phosphorylation of eIF2alpha and upregulation o

118 This demonstrates that Atf6 can play both protective and pathological roles in

119 linked to the activation of a specific arm, ATF6/CHOP, of the unfolded protein response pathway.

120 Cardiac myocyte-specific deletion of Atf6 (ATF6 cKO [conditional knockout]) blunted transverse aort

121 rtrophy in wild type mouse hearts but not in ATF6 cKO hearts.

122 ted virus 9- RHEB restored cardiac growth to ATF6 cKO mice subjected to transverse aortic constrictio

123 c analysis showed that the luminal region of ATF6 confers SEL1L dependence on type I transmembrane pr

124 A hybrid protein with the ATF6 cytoplasmic domain replaced by a constitutive sorti

125 tivity; class 2 ATF6 mutants bear the entire ATF6 cytosolic domain with fully intact transcriptional

126 grams, supporting a novel mechanism by which ATF6 decreases myocardial I/R damage.

127 ects were lost upon cardiac myocyte-specific Atf6 deletion in the heart, demonstrating the critical r

128 e to regulating the strength and duration of ATF6-dependent ERSR gene induction and cell viability.

129 nally, simulated ischemia induced MANF in an ATF6-dependent manner in neonatal rat ventricular myocyt

130 is shown to upregulate TXNDC5 via ER stress/ATF6-dependent transcriptional control in lung fibroblas

131 cause S1P has a nonredundant function in the ATF6-dependent unfolded protein response (UPR), woodrat

132 ATF6 does not appear to play a major role in type 2 diab

133 Instead, depleting larvae of active Atf6 either through a membrane-bound transcription facto

134 R exit sites and attenuated translocation of ATF6-enhanced green fluorescent protein to the nucleus.

135 The finding of activated caspase and ATF6 expression in PN within both the EF and PF groups s

136 of S2P from Golgi to ER with proteolysis of ATF6 followed by up-regulation of ER chaperones, mimicki

137 We show that during stress, ATF6 forms an interaction with COPII, the protein comple

138 The cleaved ATF6 fragment migrates to the nucleus to transcriptional

139 oth the synthesis of ATF6 and trafficking of ATF6 from the ER to the Golgi for intramembrane proteoly

140 d two compound-heterozygous mutations in the ATF6 gene (encoding activating transcription factor 6A),

141 However, ATF6 gene silencing does not result in apoptosis of mela

142 nd vascular-associated gene expression (Bip, Atf6, Hif1a, Pik3/Akt, Flt1/Vegfa, and Tgfb1), which may

143 e heart is protected from ischemic damage by ATF6; however, ERAD has not been studied in the cardiac

144 ER stress markers, including atf6, hspa5, calr, and xbp1, are selectively up-regulate

145 ear accumulation of transcriptionally active ATF6, improving prosurvival UPR function in striatal neu

146 Knockdown of ATF6 in cardiac myocytes subjected to I/R increased reac

147 METHODS AND Knockdown of ATF6 in cardiac myocytes subjected to I/R increased reac

148 in the catalase gene and were shown to bind ATF6 in cardiac myocytes, which increased catalase promo

149 d cardiac function, demonstrating a role for ATF6 in compensatory myocyte growth.

150 demonstrating critical roles for endogenous ATF6 in ischemia-mediated ER stress activation and cell

151 t, demonstrating the critical role played by ATF6 in mediating pharmacologically activated proteostas

152 genes, including GRP78; however, the role of ATF6 in mediating this induction has not been examined.

153 ablation of XBP1 or inducible expression of ATF6 in mice aggravates DN.

154 Mechanistically, knockdown of ATF6 in neonatal rat ventricular myocytes blocked phenyl

155 ssociated ATF6 with a coordinate increase of ATF6 in nuclear fractions.

156 ssociated transcription factors XBP1s and/or ATF6 in the absence of stress recapitulates the selectiv

157 expresses a conditionally activated form of ATF6 in the heart.

158 f the ERAD machinery, is robustly induced by ATF6 in the mouse heart.

159 Blockade of IRE1alpha or ATF6 in the oxygen-induced retinopathy or choroidal neov

160 target genes such as SERCA2b and/or through ATF6-independent genes (TGF-beta1, ADAM8).

161 g that dec-RRLL-CMK induces cell death in an ATF6-independent manner.

162 activating transcription factor 4 (ATF4) and ATF6 indicating potential contributions of the unfolded

163 METHODS AND In the present study, activated ATF6 induced Derl3 in cultured cardiomyocytes, and in th

164 Finally, ATF6 induced RHEB in response to growth factors, but not

165 l (AdV)-mediated overexpression of activated ATF6 induced the RCAN1 promoter, up-regulated RCAN1 mRNA

166 Many of the proteins encoded by the ATF6-induced oxidative stress genes identified here resi

167 We determined that ATF6 induces liver X receptor-alpha (LXRalpha), an Mertk

168 urther, overexpression of the active form of ATF6 induces protective UPR and improves insulin signali

169 gulator of calcineurin 1 (RCAN1), as a novel ATF6-inducible gene that encodes a known regulator of ca

170 ss response genes not previously known to be ATF6-inducible.

171 e (PERK), activating transcription factor-6 (ATF6), inositol requiring enzyme 1alpha (IRE1alpha), and

172 tion of ER stress with PBA and siRNA against ATF6, IRE1, and GRP78 mitigated ox-LDL-induced CD36 prot

173 by three ER transmembrane proteins including ATF6, IRE1, and PERK.

174 The ER stress proteins PERK, ATF4, ATF6, IRE1alpha, and CHOP were upregulated in RGC-5 cell

175 ions and the expression of ER stress sensors Atf6, Ire1alpha, Perk, their downstream effectors Grp78/

176 analysis revealed that the luminal region of ATF6 is a determinant for SEL1L-dependent degradation.

177 ATF6 is a key regulator of the unfolded protein response

178 Thus, ATF6 is a previously unrecognized link between growth st

179 ot required for CHOP expression, but instead ATF6 is a primary inducer.

180 This is the first study to show that ATF6 is activated by ischemia but inactivated upon reper

181 However, it is not known whether ATF6 is activated, and if so, what its function is durin

182 srupted ER/Golgi membrane network, where pro-ATF6 is activated.

183 Pharmacological activation of ATF6 is also protective in renal and cerebral ischemia/r

184 Upon ER stress, ER-associated ATF6 is cleaved; the resulting active cytosolic fragment

185 The transcription factor ATF6 is held as a membrane precursor in the endoplasmic

186 this response nor whether it is mediated by ATF6 is known.

187 ATF6 is retained in the ER by association with the chape

188 nsory proteins-PERK (PEK/EIF2AK3), IRE1, and ATF6-is activated by ER stress.

189 However, compared with wild-type, ATF6 knockout hearts showed increased damage and decreas

190 m wild-type but not in cardiac myocytes from ATF6 knockout mice.

191 verexpression of catalase, in vivo, restored ATF6 knockout mouse heart function to wild-type levels i

192 Under nonstressed conditions, wild-type and ATF6 knockout mouse hearts were similar.

193 ncing hepatocyte Plat Conversely, hepatocyte-ATF6-knockout mice show decreases in these parameters.

194 The density of ATF6 labeling was not different between the EF and PF gr

195 activates activating transcription factor 6 (ATF6), leading to the increased binding of ATF6 on the m

196 e findings identify a macrophage CaMKIIgamma/ATF6/LXRalpha/MerTK pathway as a key factor in the devel

197 BP1u as a potent repressor of both XBP1s and ATF6-mediated activation.

198 ere, we examined the effects of blocking the ATF6-mediated ER stress response on ischemia/reperfusion

199 non-toxic small molecules that phenocopy the ATF6-mediated reprogramming of the ER proteostasis envir

200 To examine the mechanism of ATF6-mediated survival in vivo, we developed a transgeni

201 Atf6(-/-) mice have normal retinal morphology and functi

202 Consistent with these observations, the Atf6(-/-) mice were highly susceptible to lethal bacteri

203 sponse to endoplasmic reticulum (ER) stress, ATF6 migrates from the ER to Golgi to undergo regulated

204 ption factor peptidase site 1 mutation or an atf6 morpholino injection protected them against steatos

205 olysis and transcriptional activity; class 2 ATF6 mutants bear the entire ATF6 cytosolic domain with

206 ATF6 mutants defective for p38 MAPK phosphorylation fail

207 ven in the absence of ER stress; and class 3 ATF6 mutants have complete loss of transcriptional activ

208 distinct molecular pathomechanisms: class 1 ATF6 mutants show impaired ER-to-Golgi trafficking and d

209 ted the function of achromatopsia-associated ATF6 mutations and found that they group into three dist

210 The ACHM-associated ATF6 mutations attenuate ATF6 transcriptional activity i

211 ATF6 mutations in patients with achromatopsia include mi

212 Our findings reveal that human ATF6 mutations interrupt distinct sequential steps of th

213 blasts from patients with class 1 or class 3 ATF6 mutations show increased cell death in response to

214 pathology of achromatopsia in patients with ATF6 mutations.

215 This was accompanied by diminished ATF6 nuclear localization in stressed senescent cells.

216 To examine the effect of ATF6 on rhodopsin, wild-type (WT) or mutant rhodopsins w

217 (ATF6), leading to the increased binding of ATF6 on the myocardin promoter and increased its express

218 level of activating transcription factor 6 (ATF6), one of the transcription factors for ER chaperone

219 Mice gene-deleted for Atf6 or Atf6b were subjected to 2 weeks of transverse ao

220 autophagic response in cells lacking either ATF6 or C/EBP-beta.

221 study indicates that selectively activating ATF6 or PERK prevents mutant rhodopsin from accumulating

222 se strategies, it was examined how selective ATF6 or PERK signaling affected the fate of WT and mutan

223 s against activating transcription factor 6 (ATF6) or activated caspase 12 and calbindin.

224 Moreover, dominant-negative ATF6, or ATF6-targeted miRNA blocked sI-mediated grp78 i

225 wn or pharmacological blockade of IRE1alpha, ATF6, or CRYAB increased intracellular VEGF degradation

226 Inhibition of IRE1alpha, ATF6, or CRYAB resulted in an approximately 40% reductio

227 gic strategies to selectively modulate IRE1, ATF6, or PERK signaling to both ameliorate pathologic im

228 cell death, both of which were mitigated by ATF6 overexpression.

229 cell death, both of which were mitigated by ATF6 overexpression.

230 /R, as did adeno-associated virus 9-mediated ATF6 overexpression.

231 the expression levels of GRP78 (p < 0.0001), ATF6 (p < 0.0001), and PERK (p < 0.0001) were significan

232 Additionally, inhibition of the ATF6 pathway by intrathecal treatment with ATF6 siRNA re

233 It was concluded that activation of the ATF6 pathway of the UPR limits ATZ-dependent cell toxici

234 GECs, iPLA2gamma amplified activation of the ATF6 pathway of the UPR, resulting in up-regulation of E

235 , acute ATF6alpha knockdown markedly reduced ATF6-pathway target gene expression under both basal and

236 and late DENV-2 infection, the IRE1-XBP1 and ATF6 pathways are activated, respectively.

237 gether, these data suggest that the XBP1 and ATF6 pathways are simultaneously activated in islet cell

238 evidence for activation of the IRE1alpha or ATF6 pathways in Cx50D47A-expressing lenses.

239 t parallel XBP1 (X box-binding protein 1) or ATF6 pathways, using siRNA and/or overexpression plasmid

240 o concomitant activation of the PERK and the ATF6 pathways.

241 (IRE1) and activated transcription factor 6 (ATF6) pathways with no concomitant significant activatio

242 n P23H rats, photoreceptor levels of cleaved ATF6, pEIF2alpha, CHOP, and caspase-7 were much higher t

243 activation of three transmembrane receptors, ATF6, PERK and IRE1alpha.

244 ing modest increases in the level of nuclear ATF6, phosphorylated eukaryotic initiation factor 2alpha

245 ated ox-LDL-induced nuclear translocation of ATF6, phosphorylation of IRE1 and up-regulation of XBP1

246 The inverse correlation between DACH1 and ATF6/PLAT is conserved in human liver.

247 A loss of Atf6 prevents steatosis caused by chronic ER stress but

248 linide blocked this interaction and enhanced ATF6 processing and nuclear accumulation of transcriptio

249 We previously showed that activating ATF6 protected the hearts of ATF6 transgenic mice from E

250 APB or VAPB(P56S) attenuates the activity of ATF6-regulated transcription and the mutant protein VAPB

251 Thus, ATF6 represents a novel type of ERAD-Lm substrate requir

252 Thus, pharmacologic activation of ATF6 represents a proteostasis-based therapeutic strateg

253 se in the ER, indicating that degradation of ATF6 requires proper mannose trimming.

254 ATF6 serves an important role as a previously unapprecia

255 the evidence demonstrating the importance of ATF6 signaling in protecting different tissues against i

256 ATF6 signaling may be especially useful in treating reti

257 ole for DREAM silencing in the activation of ATF6 signaling, which promotes early neuroprotection in

258 ATF6 significantly reduced T17M, P23H, Y178C, C185R, D19

259 e ATF6 pathway by intrathecal treatment with ATF6 siRNA reduced pain behaviors and BIP expression in

260 ER stress-activated lipogenesis through the ATF6/SREBP-1c pathway in vitro.

261 ets of CREB/ATF family, heat-shock factor 1, ATF6, SRF, and E2F1 transcription factors.

262 an ER luminal -SH reactive bond controls BiP-ATF6 stability and access of ATF6 to the COPII budding m

263 RHEB (Ras homologue enriched in brain) as an ATF6 target gene in the heart.

264 6 that do not induce growth, indicating that ATF6 target gene induction is stress specific.

265 The ATF6 target gene SERCA2b, implicated in airway remodelin

266 se results demonstrate that RCAN1 is a novel ATF6 target gene that may coordinate growth and ER stres

267 ivo in airway remodeling potentially through ATF6 target genes such as SERCA2b and/or through ATF6-in

268 d that ER stress and ATF6 were activated and ATF6 target genes were induced in mice subjected to an a

269 Moreover, dominant-negative ATF6, or ATF6-targeted miRNA blocked sI-mediated grp78 induction,

270 the expression of a specific subset of XBP1-ATF6 targets, further illuminating the complexity of the

271 , but not in response to other activators of ATF6 that do not induce growth, indicating that ATF6 tar

272 Unlike ATF6, the two other UPR pathways, i.e. inositol-requirin

273 ATF6 then induces mesencephalic astrocyte-derived neurot

274 The ability of ATF6 to induce RCAN1 in vivo was replicated in cultured

275 he potential for pharmacologically targeting ATF6 to intervene in such diseases.

276 nd controls BiP-ATF6 stability and access of ATF6 to the COPII budding machinery.

277 established the binding of the UPR-activated ATF6 transcription factor to this region during ER stres

278 The ACHM-associated ATF6 mutations attenuate ATF6 transcriptional activity in response to ER stress.

279 ieved through preferential activation of the ATF6 transcriptional program, is a promising strategy to

280 that activating ATF6 protected the hearts of ATF6 transgenic mice from ER stresses.

281 Upon ER stress, transcription factor ATF6 translocates from the ER to Golgi, where it is sequ

282 ; the resulting active cytosolic fragment of ATF6 translocates to the nucleus, binds to ER stress res

283 otine also attenuated endogenously expressed ATF6 translocation and phosphorylation of eukaryotic ini

284 acellular MUC1-fs accumulation activated the ATF6 unfolded protein response (UPR) branch.

285 osphorylates a critical threonine residue in ATF6 upstream of its DNA binding domain.

286 phorylation of eIF2alpha and nuclear form of ATF6 was detected in CS-exposed animals.

287 In addition, endogenous ATF6 was markedly stabilized in wild-type cells treated

288 ATF6 was rapidly degraded by proteasomes, consistent wit

289 pitulates the ER-stress induced transport of ATF6, we show that no cytoplasmic proteins other than CO

290 We found that ER stress and ATF6 were activated and ATF6 target genes were induced i

291 anscription factor 4 (ATF4), and cleavage of ATF6 were significantly increased in cells expressing D1

292 with the induction of CHOP and activation of ATF6, whereas bortezomib resulted in the induction of CH

293 cation of activating transcription factor 6 (ATF6), which is part of the UPR.

294 ER stress activates the transcription factor ATF6, which induces expression of proteins targeted to t

295 cardiac hypertrophy activates ER stress and ATF6, which induces RHEB and activates mTORC1.

296 way in which the corepressor DACH1 represses ATF6, which is an inducer of the tPA gene Plat Hepatocyt

297 anistically, gene array analysis showed that ATF6, which is known to induce genes encoding ER protein

298 ne BiP at mRNA and protein level, as well as atf6, which ultimately led to induction of the important

299 naling molecules: Ire-1alpha/beta, PERK, and ATF6, whose function is to facilitate adaption to the en

300 ed a reduction in the level of ER-associated ATF6 with a coordinate increase of ATF6 in nuclear fract

301 d in the induction of CHOP and activation of ATF6 with minimal effects on XBP1.

302 on of XBP1 and robust cleavage activation of ATF6, with abnormal regulation of calreticulin levels.

303 pathways, including activation of eIF2alpha, ATF6, xbp-1 splicing, as well as caspase activation.