ライフサイエンスコーパス: ATF6

1 including activating transcription factor 6 (ATF6).

2 E-1), and activating transcription factor 6 (ATF6).

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

4 cation of activating transcription factor 6 (ATF6).

5 APK) pathway for controlling the activity of ATF6.

6 eased expression of the transcription factor ATF6.

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

8 s affected by the inhibition of IRE1alpha or ATF6.

9 F6f, the transcriptional activator domain of ATF6.

10 intramembrane proteolysis and activation of ATF6.

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

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

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

14 eavage of the mammalian transcription factor ATF6.

15 t with the ER-localized transcription factor ATF6.

16 sses a novel conditionally activated form of ATF6.

17 and activation of the transcription factor, ATF6.

18 located in a functionally important part of ATF6.

19 d is mediated in part by the nuclear form of ATF6.

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

21 nfirms accumulation of precursor SREBP-1 and ATF6.

22 protection was reversed by dominant-negative ATF6.

23 ta cell proliferation, through activation of ATF6.

24 d the ER stress response regulators XBP1 and ATF6.

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

26 of activating transcription factors ATF4 and ATF6.

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

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

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

30 also inositol requiring kinase 1 (IRE1) and ATF6, 3 pathways of the unfolded protein response (UPR).

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 The UPR-mediated activation of ATF6 (Activation of Transcription Factor 6) induces cyto

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

40 6S) appears to be a more potent inhibitor of ATF6 activity.

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

42 asmic reticulum (ER)-transmembrane proteins, ATF6 alpha and ATF6 beta, are cleaved during the ER stre

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

44 The resulting N-terminal fragments (N-ATF6 alpha and N-ATF6 beta) have conserved DNA-binding d

45 activation domain or DNA-binding domain of N-ATF6 alpha exhibited loss of function and increased expr

46 We previously showed that N-ATF6 alpha is a rapidly degraded, strong transcriptional

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

48 Fusing N-ATF6 alpha to the mutant estrogen receptor generated N-A

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

50 pression, but in the presence of tamoxifen N-ATF6 alpha-MER exhibited gain-of-function and low expres

51 to the mutant estrogen receptor generated N-ATF6 alpha-MER, which, without tamoxifen exhibited loss-

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

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

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

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

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

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

58 reticulum (ER) stress-induced activation of ATF6, an ER membrane-bound transcription factor, require

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 show that YY1 is an essential coactivator of ATF6 and uncover their specific interactive domains.

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

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

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

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

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

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

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

87 e (PERK), activating transcription factor 6 (ATF6), and inositol-requiring enzyme 1 (IRE-1), to favor

88 vation of activating transcription factor 6 (ATF6), and protein kinase R-like endoplasmic reticulum (

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

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

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

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

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

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

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

96 promoter is enhanced by the nuclear form of ATF6, and this synergy is further potentiated by YY1.

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

98 pha, we provide direct evidence that YY1 and ATF6 are required for optimal stress induction of Grp78.

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

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

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 ssion of a novel tamoxifen-activated form of ATF6, ATF6-MER.

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 ver, siRNA-mediated knock-down of endogenous ATF6 beta increased GRP78 promoter activity and GRP78 ge

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

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

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

111 ing N-terminal fragments (N-ATF6 alpha and N-ATF6 beta) have conserved DNA-binding domains and diverg

112 (ER)-transmembrane proteins, ATF6 alpha and ATF6 beta, are cleaved during the ER stress response (ER

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

114 ATF6 binds to ER stress response elements in target gene

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

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

117 Second, ATF6 bound at similar levels to wild-type BiP and a BiP

118 heart during I/R and that, as a result, the ATF6 branch of the UPR may induce expression of proteins

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

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

121 tion and that ER stress dissociates BiP from ATF6 by actively restarting the BiP ATPase cycle.

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

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

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

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

126 lded proteins causes dissociation of the BiP-ATF6 complex in stressed cells.

127 ally postulated that dissociation of the BiP-ATF6 complex is a result of the competitive binding of m

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

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

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

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

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

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

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

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

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

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

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

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

140 otein kinase and the transcription regulator ATF6 following up to 6 h of proteasome inhibitor treatme

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

142 The cleaved ATF6 fragment migrates to the nucleus to transcriptional

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

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

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

146 P12 gene and into the 5' end of the adjacent ATF6 gene.

147 f ATF4 or an active mutant form of XBP-1 and ATF6 had the opposite affect.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 evealing a broader than anticipated role for ATF6 in this signaling network.

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

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

166 by ATF6, were activated by a virus-induced, ATF6-independent mechanism.

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

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

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

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

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

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

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

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

175 ER transmembrane components, IRE1, PERK, and ATF6, initiate distinct UPR signaling branches.

176 R stress: activating transcription factor 6 (ATF6), inositol requiring 1 (IRE1), and PKR-like endopla

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

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

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

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

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

182 ATF6 is a key regulator of the unfolded protein response

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

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

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

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

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

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

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

190 Since the expression of YY1 as well as ATF6 is ubiquitous in the mouse embryo, activation of th

191 Activating transcription factor 6 (ATF6) is important for protective cell response to accum

192 Activating transcription factor 6 (ATF6) is located within the region of linkage to type 2

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

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

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

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

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

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

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

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

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

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

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

204 When NTG and ATF6-MER TG mice were treated with or without tamoxifen

205 of a novel tamoxifen-activated form of ATF6, ATF6-MER.

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

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

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

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

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

211 ATF6 mutants defective for p38 MAPK phosphorylation fail

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

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

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

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

216 ATF6 mutations in patients with achromatopsia include mi

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

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

219 pathology of achromatopsia in patients with ATF6 mutations.

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

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

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

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

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

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

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

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

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

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

230 l that is based on dynamic binding of BiP to ATF6, our data reveal relatively stable binding.

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

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

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

234 ted levels of GRP78, IRE1alpha, XBP-1, ATF4, ATF6, p-PERK, p-eIF2alpha, and GADD34 and reduced levels

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

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

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

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

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

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

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

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

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

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

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

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

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 The three UPR branches (IRE1, PERK, and ATF6) promote cell survival by reducing misfolded protei

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

251 To examine whether ATF6 protects the myocardium from I/R injury in the hear

252 d splicing of XBP1 mRNA; and cleavage of the ATF6 protein in NBD rat brains.

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

254 ose that stable BiP binding is essential for ATF6 regulation and that ER stress dissociates BiP from

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

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

257 ATF6 serves an important role as a previously unapprecia

258 ATF6 signaling may be especially useful in treating reti

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

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

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

262 subjects and 182 control subjects, nor were ATF6 SNPs associated with altered insulin secretion or i

263 tion, and activating transcription factor 6 (ATF6) splicing.

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

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

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

267 The ATF6 target gene SERCA2b, implicated in airway remodelin

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

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

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

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

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

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

274 vivo binding of YY1 and the nuclear form of ATF6 to the ERSE.

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

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

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

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

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

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

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

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

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

284 an ER Ca2+ ATPase inhibitor, the response of ATF6 was markedly delayed.

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

286 ATF6 was rapidly degraded by proteasomes, consistent wit

287 duced activation of the transcription factor ATF6 was suppressed in HCMV-infected cells; however, spe

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

289 Functionally important segments of ATF6 were sequenced in 15 diabetic and 15 nondiabetic Pi

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

291 cific chaperone genes, normally activated by ATF6, were activated by a virus-induced, ATF6-independen

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

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

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

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

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

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

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