ライフサイエンスコーパス: XBP1

1 limp-1 (PRDM1), and X-box binding protein 1 (XBP1).

2 ranscription factor X-box binding protein 1 (XBP1).

3 ranscription factor X-box binding protein 1 (XBP1).

4 1alpha-dependent decay (RIDD) independent of XBP1.

5 transmembrane sensor IRE1 and its substrate XBP1.

6 nism that requires the transcription factor, XBP1.

7 emerge from Paneth-cell-specific deletion of Xbp1.

8 rogression, including TP53, BTG1, MKI67, and XBP1.

9 cing, occurring after depletion of unspliced XBP1.

10 on of the alternatively spliced mRNA variant XBP1 (16-fold).

11 tic inactivation of X-box binding protein-1 (Xbp1), a transcription factor activated during endoplasm

12 ess-induced mRNA splicing, including that of Xbp1, a cellular stress sensor.

13 Xbp1, a key mediator of the unfolded protein response (U

14 We aim to determine the role of hepatic Xbp1, a key mediator of the UPR, in controlling the adap

15 R1 mRNA expression and increased splicing of XBP1, a known IRE-alpha substrate, thereby pointing towa

16 rolysis of xylan are recognized and bound by XBP1, a putative solute-binding protein, likely for tran

17 canonical fibrogenic driver, suggesting that XBP1 activates a specific subset of fibrogenesis pathway

18 ddition, doxorubicin significantly inhibited XBP1 activation in CD138(+) tumor cells isolated from MM

19 A small molecule inhibitor of ERN1-mediated XBP1 activation induced selective cell death of patient-

20 icin as an in vitro and in vivo inhibitor of XBP1 activation, a previously unknown activity for this

21 XBP1 activation, fueled by lipid peroxidation byproducts

22 show that SEC63 function regulates IRE1alpha/XBP1 activation, SEC63 and XBP1 are required for GPS cle

23 pression is reduced to a level that prevents XBP1 activation.

24 us protein (CHOP), X2-Box-binding protein 1 (XBP1), activator protein 1 (AP1), SMAD, CCAAT/enhancer-b

25 IRE1-signaling pathway, by expression of the XBP1-active form, compromised GCB DLBCL tumor growth in

26 Effects on XBP1 activity were not detected in these cells; however,

27 r cell lines that have lower basal IRE1alpha-XBP1 activity.

28 induced by phenols, while overexpression of XBP1 alone increased their expression.

29 GATA, and the ER stress response regulators XBP1 and ATF6.

30 AICDA, NFIL3, IRF4, XBP1 and BATF3 shared a profile with several genes invol

31 olded protein response transcription factors XBP1 and CHOP nor the TLR4 adaptor molecule MyD88 is nec

32 ctor 6-mediated arm of this response through Xbp1 and downstream activation of the endoplasmic reticu

33 phosphorylation of IRE1 and up-regulation of XBP1 and GRP78.

34 a mediator of these activities, and identify XBP1 and its splicing to be novel therapeutic targets.

35 10 genes selected by dwgLASSO, UBE2S, SALL2, XBP1 and KIAA0922 have been confirmed by literature surv

36 We now show a direct link between the XBP1 and NF-kappaB survival pathways in driving the cell

37 Of note, both the IRE1/XBP1 and PERK/eIF2alpha arms of unfolded protein respons

38 the activation loop show decreased specific Xbp1 and promiscuous RNase splicing activity relative to

39 of HNF4alpha caused decreased expression of XBP1 and reduced cellular ER networks.

40 nce-specific transcription factors including Xbp1 and Stb3.

41 through C-terminal domain with the unspliced XBP1 and the inositol requiring enzyme 1 alpha in the en

42 Delivery of DNA vaccines encoding XBP1 and tumor Ag to skin DC resulted in increased IFN-a

43 enotype, with suppression of Blimp, IRF4 and XBP1 and upregulation of BCL6, whereas introduction of p

44 ER Ca(2+) signaling; we show that diminished XBP1 and/or HNF4alpha in beta-cells led to impaired ER C

45 ), up-regulation of X-box-binding protein 1 (XBP1) and glucose-regulated protein 78 (GRP 78), and nuc

46 rphisms in candidate genes with known (i.e., Xbp1) and unknown roles in ER stress.

47 dent on the activity of transcription factor XBP1, and ANG promoted cellular adaptation to ER stress

48 he cell through the activation of PERK, IRE1/XBP1, and ATF6.

49 sion of key plasma cell genes such as Prdm1, Xbp1, and CD138.

50 n of multiple key factors, including Blimp1, Xbp1, and CXCR4, and is therefore critical for establish

51 mice, we found that PH induces expression of XBP1, and that this activity requires interleukin 6.

52 eukaryotic initiation factor 2alpha, nuclear XBP1, and the downstream proapoptotic effector nuclear C

53 gulates IRE1alpha/XBP1 activation, SEC63 and XBP1 are required for GPS cleavage and maturation of PC1

54 the IRE1alpha-dependent transcription factor XBP1, are dispensable for this signaling.

55 These findings further imply XBP1 as a relevant target for cancer therapy.

56 ion of the myc pathway and downregulation of XBP1 as likely mediators of the host transcriptional cha

57 the UPR pathway and its downstream effector XBP1 as novel therapeutic targets to overcome drug resis

58 s the mRNA encoding the transcription factor Xbp1 at a dual stem-loop (SL) structure, leading to Xbp1

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

60 enin reflected the activity of the IRE1alpha-XBP1 axis in allografts.

61 notype, marked by induction of the IRE1alpha/XBP1 axis of the unfolded protein response (UPR) and cul

62 issue showed that at 6 hours after PH, liver XBP1 became bound to a large set of genes implicated in

63 target genes that contain adjacent MIST1 and XBP1 binding sites.

64 At this time point, XBP1 bound the promoter of the signal transducer and act

65 Although the mammalian IRE1alpha-XBP1 branch of the cellular unfolded protein response ha

66 Activation of the IRE1alpha-XBP1 branch of the unfolded protein response (UPR) has b

67 Our findings reveal a key function for the XBP1 branch of the UPR in TNBC and indicate that targeti

68 ith its inhibitory activity on the IRE1alpha-XBP1 branch of the UPR, doxorubicin displayed more poten

69 ficiency selectively activates the IRE1alpha-XBP1 branch of UPR and that SEC63 exists in a complex wi

70 ed by ER stress and X-box-binding protein 1 (XBP1) but not by activating transcription factor 6 alpha

71 ne expression is induced during ER stress by XBP1, but as ER stress subsides, MIST1 serves as a feedb

72 nd that ablation of the transcription factor XBP1, but not ATF4, significantly delay locomotor recove

73 Reconstitution of XBP1 by Ad-XBP1s gene transfer significantly improved an

74 Expression of XBP1 by hepatocytes increased immediately after PH (prim

75 These results suggest that XBP1 can function via growth factor signaling pathways t

76 age and maturation of PC1, and activation of XBP1 can protect against polycystic disease in the setti

77 rence, we solved the co-crystal structure of XBP1 complexed with xylotriose to a 1.8-A resolution.

78 Ldlr knockout mice transplanted with XBP1-conditional knockout (or wild-type control litterma

79 In Ldlr/XBP1-conditional knockout mice, serum levels of IgG, IgE

80 XBP1 (X-box binding protein-1) floxed mice (XBP1-conditional knockout), with antibody-mediated deple

81 mediators, such as X-box-binding protein 1 (XBP1), confer genetic risk for inflammatory bowel diseas

82 f XBP1 increased, whereas siRNA knockdown of XBP1 considerably reduced, PRNP and ERLEC1 mRNA levels i

83 , Cre-mediated deletion of Hspa5, Prdm1, and Xbp1 consistently induces cellular stress and cell death

84 These data indicate that hepatic XBP1 controls the adaptive response of the UPR and is cr

85 Here we show that IRE1/XBP1 controls the induction of autophagy/ERAD(II) during

86 anscription factor, X-box-binding protein-1 (XBP1), controls the development and maintenance of the e

87 l knock-out (XBP1eko) mice demonstrated that XBP1 deficiency in ECs reduced the basal level of LC3bet

88 Together, these data indicate that XBP1 deficiency in pancreatic alpha-cells induces altere

89 with hindlimb ischemia models revealed that XBP1 deficiency in SMCs significantly attenuated angioge

90 In regenerating livers, XBP1 deficiency leads to endoplasmic reticulum stress an

91 XBP1 deficiency led to decreased macrophage recruitment,

92 Down-regulation of ER UPR in XBP1 deficient cells increases cyotosolic ALIS formation

93 and the attenuation of protein synthesis in XBP1-deficient livers.

94 ctin receptor (Prlr) and ErbB4 expression in Xbp1-deficient mammary epithelium.

95 CReP expression was markedly suppressed in XBP1-deficient mice livers due to hyperactivated IRE1alp

96 Additionally, epithelial Xbp1 deletion induces endoplasmic reticulum (ER) stress

97 Accordingly, DC-specific XBP1 deletion or selective nanoparticle-mediated XBP1 si

98 Xbp1(DeltaIEC) mice show autophagosome formation in hypo

99 Here we show that impairment in either UPR (Xbp1(DeltaIEC)) or autophagy function (Atg16l1(DeltaIEC)

100 y be utilized clinically to target IRE1alpha-XBP1-dependent tumors such as MM.

101 her, our findings provide a new paradigm for XBP1-dependent UPR regulation and position MIST1 as a po

102 Microarray analysis of IRE1alpha- and XBP1-depleted cells, validation using RNA cleavage assay

103 -induced autophagy response, whereas spliced XBP1 did not induce transcriptional activation of a trun

104 We determined that XBP1 directly binds the promoter and induces transcripti

105 These findings indicate that IRE1-XBP1 downregulation distinguishes GCB DLBCL from other D

106 s downstream target X-box-binding protein 1 (XBP1) drive B-cell differentiation toward plasma cells a

107 scriptional regulatory network revealed that XBP1 drives TNBC tumorigenicity by assembling a transcri

108 Importantly, data from arterial vessels from XBP1 EC conditional knock-out (XBP1eko) mice demonstrate

109 d increased levels of the ER stress reporter Xbp1-EGFP.

110 Enforced expression of Helios or Xbp1 elicited distinct signatures, but Eos, IRF4, Satb1,

111 Concomitant inactivation of both SEC63 and XBP1 exacerbated the polycystic kidney phenotype in mice

112 , the enzyme responsible for ligation of two XBP1 exons remains unknown.

113 Knocking down XBP1 expression also increased NO concentration, as dete

114 Knocking down XBP1 expression by transducing RAW 264.7 cells with the

115 The inhibition of XBP1 expression caused a reduced up-regulation of DDR me

116 XBP1 expression regulates the unfolded protein response,

117 Restoring XBP1 expression was sufficient to completely rescue GSIS

118 important for many aspects of Ab secretion, XBP1 expression, and the UPR.

119 r Factor 4alpha (HNF4alpha) directly induces XBP1 expression.

120 -specific Xbp1 knockout mice (Xbp1(LKO)) and Xbp1(fl/fl) control mice were subjected to varying level

121 By 24 h, Xbp1(fl/fl) controls showed complete resolution of UPR a

122 Xbp1(LKO) and Xbp1(fl/fl) mice showed robust and equal activation of t

123 lator of the UPR master transcription factor XBP1 for a portion of target genes that contain adjacent

124 These consequences of hypomorphic Xbp1 function are associated with an increased propensit

125 We report here that hypomorphic Xbp1 function instructs a multilayered regenerative resp

126 ts of patients with TNBC revealed a specific XBP1 gene expression signature that was highly correlate

127 nitored by measuring HSPA5, CHOP and spliced XBP1 gene expression, and type I IFN by measuring IFNB1

128 The transcription factor XBP1 has been linked to the development of highly secret

129 In cirrhotic livers, activation of the XBP1-Hrd1 arm of ER stress transcriptionally up-regulate

130 s patients, we observed up-regulation of the XBP1-Hrd1 arm of the ER stress response pathway and down

131 Xbp1 splicing, and deficiency of Archease or Xbp1 impeded axon regeneration in Drosophila.

132 Similarly, human XBP1 improved the capacity of human blood- and skin-deri

133 In contrast, silencing XBP1 in adult animals triggered chronic ER stress and do

134 To evaluate the role of XBP1 in alpha-cells, we created complementary in vivo (a

135 ignaling activities of spliced and unspliced XBP1 in breast cancer, establish NF-kappaB to be a media

136 on in various human tumours, but the role of XBP1 in cancer progression in mammary epithelial cells i

137 expression of Grp78, ATF6, ATF4, and spliced XBP1 in CD8alphabeta(+) IEL but not in CD8alphaalpha(+)

138 n response components ATF4, CHOP, GRP78, and XBP1 in CP.

139 data support an important intrinsic role for XBP1 in DC for effective cross-priming and orchestration

140 tedly selective and absolute requirement for XBP1 in eosinophil differentiation without an effect on

141 However, the direct function of Xbp1 in epithelial cells during mammary gland developmen

142 Conversely, deficiency of XBP1 in healthy donor BMSCs displayed a range of effects

143 er and promoter sequences for theIfnbgene by XBP1 in infected RAW 264.7 cells.

144 This study reveals an unexpected role for Xbp1 in suppressing tumor formation through restraint of

145 As such, Xbp1 in the intestinal epithelium not only regulates loc

146 Here we report that the loss of Xbp1 in the mammary epithelium through targeted deletion

147 Here we show that constitutive activation of XBP1 in tumor-associated DCs (tDCs) drives ovarian cance

148 Cell, Cubillos-Ruiz et al. demonstrate that XBP1 in tumor-infiltrating dendritic cells blunts anti-t

149 ranscription factor X box-binding protein 1 (XBP1) in DC appears to play a decisive role in promoting

150 ranscription factor X-box binding protein-1 (Xbp1) in intestinal epithelial cells, the human ortholog

151 ranscription factor X-box binding protein 1 (XBP1) in liver regeneration using genome-wide chromatin

152 pmental ablation of X-Box binding protein 1 (XBP1) in the nervous system, a key regulator of the unfo

153 Overexpression of XBP1 increased, whereas siRNA knockdown of XBP1 consider

154 Finally, loss of both Sec63 and Xbp1 induced apoptosis in podocytes, which associated wi

155 Ectopic overexpression of XBP1 induced collagen 1-alpha expression in HSCs, which

156 BECLIN-1 deficiency in ECs abolished the XBP1-induced autophagy response, whereas spliced XBP1 di

157 These findings suggest that the loss of Xbp1 induces a terminal UPR which blocks proliferation a

158 XBP1 induces transcription of genes involved in protein

159 XBP1 induction accompanied both culture-based HSC activa

160 breast cancer cell line models, depletion of XBP1 inhibited tumour growth and tumour relapse and redu

161 Co-treatment with XBP1 inhibitors reduced IL6 and IL8 production induced b

162 mals, IRE1alpha has been known to cleave the XBP1 intron.

163 induces ER stress and P300 activity via the XBP1/IRE1 pathway.

164 Here we report that XBP1 is activated in TNBC and has a pivotal role in the

165 However, whether XBP1 is involved in EC-SMC interaction remains unclear.

166 XBP1 is part of the ER stress response, and when activat

167 and activity of the UPR downstream effector XBP1 is regulated positively by STAT5 and negatively by

168 X-box binding protein 1 (XBP1) is a transcription factor that plays a crucial rol

169 The X-box binding protein 1 (XBP1) is believed to be a signal transducer in the endop

170 ranscription factor X-box-binding protein 1 (XBP1), is increased following exposure of melanocytes to

171 ion assays further revealed that the spliced XBP1 isoform bound directly to the BECLIN-1 promoter at

172 kout [alphaXBPKO] mice) and in vitro (stable XBP1 knockdown alpha-cell line [alphaXBPKD]) models.

173 Regenerating livers from XBP1-knockdown mice expressed high levels of a marker of

174 Livers of XBP1-knockdown mice showed reduced expression of STAT3 a

175 d complementary in vivo (alpha-cell-specific XBP1 knockout [alphaXBPKO] mice) and in vitro (stable XB

176 Liver-specific Xbp1 knockout mice (Xbp1(LKO)) and Xbp1(fl/fl) control m

177 requiring enzyme 1, an upstream activator of XBP1, leading to phosphorylation of Jun NH2-terminal kin

178 ucing RAW 264.7 cells with the short hairpin XBP1 lentiviral vector significantly reduced the parasit

179 1alpha also cleaves certain mRNAs containing XBP1-like secondary structures to promote the degradatio

180 t during acute ER stress in mammalian cells, Xbp1-like SLs within the target mRNAs are necessary for

181 Xbp1(LKO) and Xbp1(fl/fl) mice showed robust and equal a

182 Conversely, Xbp1(LKO) mice showed ongoing UPR activation associated

183 Liver-specific Xbp1 knockout mice (Xbp1(LKO)) and Xbp1(fl/fl) control mice were subjected t

184 ignalling via the insulin receptor, p85, and XBP1 maintains podocyte homeostasis, while disruption of

185 14-3-3gamma, Ywhab/14-3-3beta, Smad5, Zfp36, Xbp1, Mapk12, Snail1) were experimentally validated by i

186 demonstrated a crucial role for the IREalpha/XBP1-mediated arm of the UPR in osteoclast differentiati

187 Thus, XBP1-mediated UPR contributes to fibrogenic HSC activati

188 ha/X-box-binding protein-mediated (IRE1alpha/XBP1-mediated) branch of the UPR is highly conserved and

189 g the mRNA encoding the transcription factor Xbp1, mediates mRNA degradation in response to ER stress

190 vectors encoding small hairpin RNAs against Xbp1 messenger RNA.

191 n-conventional splicing of Hac1 (yeasts) and XBP1 (metazoans) mRNA, encoding orthologous UPR transcri

192 ate in the sequence-specific splicing of the Xbp1 mRNA and in the regulated degradation of diverse me

193 ng isoform had significantly less BLIMP1 and XBP1 mRNA and, for human pre-B cells, remained CD138 neg

194 initiated by unconventional splicing of HAC1/XBP1 mRNA during endoplasmic reticulum (ER) stress.

195 ads to unconventional, enzymatic splicing of XBP1 mRNA enabling expression of the transcription facto

196 ty that is required for specific splicing of Xbp1 mRNA leading to UPR activation.

197 rials for children and adults with ALL, high XBP1 mRNA levels at the time of diagnosis predicted poor

198 ions: tRNA ligation after intron removal and XBP1 mRNA ligation during activation of the unfolded pro

199 E1alpha promotes adaptation through splicing Xbp1 mRNA or apoptosis through incompletely understood m

200 letion of these receptors markedly decreased Xbp1 mRNA processing.

201 complex, and its co-factor archease mediate XBP1 mRNA splicing both in vitro and in vivo.

202 activated autophagic gene expression through XBP1 mRNA splicing in an inositol-requiring enzyme 1alph

203 In RtcB knockout cells, XBP1 mRNA splicing is defective during ER stress.

204 cing (mRNA-Seq), we show that unconventional Xbp1 mRNA splicing is required to increase and decrease

205 The present study provides evidence that XBP1 mRNA splicing triggered an autophagic response in E

206 These results suggest that XBP1 mRNA splicing triggers an autophagic signal pathway

207 requiring enzyme 1 alpha phosphorylation and XBP1 mRNA splicing, which was abolished by siRNA-mediate

208 cretion of 120 pg/cell/day in the absence of XBP1 mRNA splicing.

209 (RNase), a key mediator of the UPR, cleaves Xbp1 mRNA to generate a potent transcription factor adap

210 d the endoribonuclease IRE1alpha and spliced Xbp1 mRNA without inducing parallel endoplasmic reticulu

211 ositive, demonstrated upregulated BLIMP1 and XBP1 mRNA, and acquired the morphology of plasma cells.

212 phosphorylation of IRE1alpha and splicing of XBP1 mRNA, resulting in exaggerated upregulation of UPR

213 he UPR, senses misfolded protein and cleaves XBP1 mRNA, which is ligated to code for the prosurvival

214 tcB is directly required for the splicing of XBP1 mRNA.

215 es in Bip and ATF4 and reductions in spliced Xbp1 mRNA.

216 nisomycin inhibited X-box-binding protein 1 (XBP1) mRNA splicing and reduced immunoglobulin-binding p

217 1alpha) to initiate X-box-binding protein 1 (Xbp1) mRNA splicing in adult primary beta cells.

218 n the 3' UTR of the X-box binding protein 1 (XBP1) mRNA that regulates its cytoplasmic splicing and s

219 pecific cleavage of X-box binding protein 1 (XBP1) mRNA, resulting in upregulation of the unfolded pr

220 activated to splice X-box binding protein 1 (XBP1) mRNA, thereby increasing XBP1s protein, which in t

221 6, BiP, Cyclin B2, OcaB (BOB1, Pou2af1), and XBP1 mRNAs, unspliced and spliced, are severely reduced

222 cludes the expression of STAT3, IL-10, ELL2, XBP1, MYC, TERT, and ADA.

223 Without XBP1, nascent eosinophils exhibited massive defects in t

224 xplored the role of X-box binding protein 1 (XBP1), one of three UPR effector pathways and sought to

225 Podocyte-specific genetic ablation of XBP1 or inducible expression of ATF6 in mice aggravates

226 Knockdown of XBP1 or inositol requiring enzyme 1 alpha decreased endo

227 Knockdown of XBP1 or IRE1alpha by shRNA in ECs ablated endostatin-ind

228 ed that either overexpression of the spliced XBP1 or treatment with platelet derived growth factor-BB

229 Schizosaccharomyces pombe lacks both a Hac1/XBP1 ortholog and a UPR-dependent-transcriptional-progra

230 leavage of PC1 in SEC63-deficient cells, and XBP1 overexpression in vivo ameliorated cystic disease i

231 of a ketogenic diet activates the IRE1alpha-XBP1 pathway in mouse livers.

232 stogenesis, and suppression of the IRE1alpha/XBP1 pathway in these cells substantially inhibited the

233 In this study, we examined whether IRE1alpha-XBP1 pathway is a potential therapeutic target in MM usi

234 ctively, our results indicate that an intact Xbp1 pathway operating to mitigate stress in the endopla

235 ntiation through activation of the IRE1alpha/XBP1 pathway.

236 endothelial cell growth factor signaling and XBP1 pathway.

237 We conclude thatL. amazonensisactivation of XBP1 plays a critical role in infection by protecting th

238 The X-box binding protein 1 (XBP1) plays an important role in EC and SMC cellular fun

239 amers against a structured RNA, derived from XBP1 pre-mRNA, that folds as two contiguous hairpins.

240 s a feedback inhibitor, directly binding the Xbp1 promoter and repressing Xbp1 transcript production.

241 lasmic reticulum (ER) stress response factor XBP1 promotes intrinsic tumor growth directly, but wheth

242 g, gene therapy to deliver an active form of XBP1 provided neuroprotection and reduced striatal dener

243 , whereas SERCA2b overexpression reduced the Xbp1 ratio to that of wild-type controls.

244 s demonstrated an increased spliced-to-total Xbp1 ratio, whereas SERCA2b overexpression reduced the X

245 Spliced XBP1 regulated endothelial cell proliferation in a PI3K/

246 We demonstrate here that genetic ablation of XBP1 results in constitutive IRE1alpha activation in the

247 ained activation of X-box-binding protein 1 (XBP1) results in endothelial cell (EC) apoptosis and ath

248 Higher expression of CHOP and XBP1 RNAs was associated with more aggressive disease.

249 ers showing increased expression of CHOP and XBP1 RNAs, and PERK and BIP proteins, but not XBP1 splic

250 rms regulate NF-kappaB activity via ERalpha; XBP1(S) is more potent because it also directly regulate

251 erone Bip but actively blocked IRE1-mediated Xbp1(s) protein accumulation.

252 unctions beyond being a dominant negative of XBP1(S).

253 form [XBP1(U)] and the spliced active form [XBP1(S)], is a key UPR component mediating antiestrogen

254 in IRS1KO was due to protein instability of Xbp1 secondary to proteasomal degradation.

255 deletion or selective nanoparticle-mediated XBP1 silencing in tDCs restored their immunostimulatory

256 essive decline in hepatic IRE1alpha-mediated XBP1 splicing activity in both genetic (ob/ob) and dieta

257 a dual stem-loop (SL) structure, leading to Xbp1 splicing and activation.

258 ein (BiP) levels, whereas BAPTA-AM increased XBP1 splicing and BiP expression, suggesting that ER cal

259 esistant variant restored IRE1alpha-mediated XBP1 splicing and improved glucose homeostasis in vivo.

260 ite of IRE1 and selectively inactivates both Xbp1 splicing and IRE1-mediated mRNA degradation.

261 er, our results demonstrate that blockade of XBP1 splicing by inhibition of IRE1alpha endoribonucleas

262 Finally, MKC-3946 inhibited XBP1 splicing in a model of ER stress in vivo, associate

263 This study demonstrates that XBP1 splicing in SMCs can control EC migration via SMC d

264 Experimental data revealed Xbp1 splicing in the retinal ganglia cells, outer plexif

265 Paradoxically, reduced ER stress or Xbp1 splicing promotes growth arrest and premature senes

266 te that glucose activates IRE1alpha-mediated Xbp1 splicing to expand the secretory capacity of the be

267 Reduction of ER stress or Xbp1 splicing using pharmacological, genetic, and RNAi a

268 bit both chemical and bacterial induction of XBP1 splicing via bacterial translocated proteins that i

269 la Rtca and Archease had opposing effects on Xbp1 splicing, and deficiency of Archease or Xbp1 impede

270 on elongation inhibitors was unable to block XBP1 splicing, but this could be rescued by expression o

271 to the pathogen was ineffective in blocking XBP1 splicing, demonstrating the need for the elongation

272 locked pattern recognition receptor-mediated XBP1 splicing, mimicking the effects of the bacterial tr

273 BLOC1S1 cleavage is temporally separate from XBP1 splicing, occurring after depletion of unspliced XB

274 Using an XBP1 splicing-based synthetic circuit, we identify RtcB

275 The XBP1 splicing-mediated up-regulation of miR-150 might be

276 BP1 RNAs, and PERK and BIP proteins, but not XBP1 splicing.

277 XBP1 target gene signatures were significantly induced i

278 ha or the activated X-box binding protein 1 (XBP1), the canonical IRE1alpha target.

279 tly binding the Xbp1 promoter and repressing Xbp1 transcript production.

280 omains to activate mRNA splicing of adaptive XBP1 transcription factor.

281 Genome-wide mapping of the XBP1 transcriptional regulatory network revealed that XB

282 tly represses expression of PRDM1, IRF4, and XBP1, transcriptional master regulators of plasma cell (

283 nd nonspliceable forms of XBP1, we show that XBP1(U) functions beyond being a dominant negative of XB

284 e transcriptionally inactive unspliced form [XBP1(U)] and the spliced active form [XBP1(S)], is a key

285 tivating its downstream transcription factor XBP1 via an unconventional splicing mechanism.

286 that LPS activates the transcription factor XBP1 via the ER stress sensor IRE1, resulting in the ind

287 Moreover, spliced XBP1 was also markedly elevated in the ipsilateral spina

288 The UPR marker sp-XBP1 was constitutively activated in ERalphaY537S cells

289 In some mice, hepatic expression of XBP1 was knocked down by injection of adenoviral vectors

290 In mice with knockdown of XBP1, we observed of liver tissue persistent endoplasmic

291 ing novel spliced and nonspliceable forms of XBP1, we show that XBP1(U) functions beyond being a domi

292 X-box binding protein 1 (XBP1), which exists in the transcriptionally inactive un

293 riptional relationship between HNF4alpha and Xbp1 with potentially broader implications about MODYI a

294 pathway of the UPR and governs expression of XBP1 (X-box binding protein 1), a key transcription fact

295 body deficiency, B cell-specific CD79a-Cre x XBP1 (X-box binding protein-1) floxed mice (XBP1-conditi

296 ATF6 (activating transcription factor 6) or XBP1 (X-box-binding protein 1).

297 Endothelial cell-specific knockout of XBP1 (XBP1ecko) in mice retarded the retinal vasculogene

298 Enforced expression of spliced XBP1 (XBP1s) enhanced GPS cleavage of PC1 in SEC63-defic

299 nhibit the splicing of XBP1u mRNA to spliced XBP1 (XBP1s), an UPR response regulator.

300 Regulons of 7 MRs (HCLS1, ZNF823, XBP1, ZNF750, RORA, TFAP2C, and ZNF57) included >500 gen