ライフサイエンスコーパス: thapsigargin

1 e sensitivity of HAECs to both histamine and thapsigargin.

2 plasmic reticulum (ER) stress-inducing agent thapsigargin.

3 the cell death caused by the SERCA inhibitor thapsigargin.

4 e endoplasmic reticulum (ER) stress inducer, thapsigargin.

5 by the inflammatory Ca(2+)-signaling mimetic thapsigargin.

6 GRP94, and ERp72 proteins after exposure to thapsigargin.

7 icular end diastolic pressure was altered by thapsigargin.

8 cells, and it blocked cell death induced by thapsigargin.

9 anced activation of the UPR upon exposure to thapsigargin.

10 increases in mSREBP-1 and iPLA(2)beta due to thapsigargin.

11 ble to the apoptosis induced by ER stressor, thapsigargin.

12 ndoplasmic reticulum Ca-ATPase activity with thapsigargin.

13 ncreased sensitivity to apoptosis induced by thapsigargin.

14 y carrot, produces the highly toxic compound thapsigargin.

15 ition when Ca(2)+ release was prevented with thapsigargin.

16 etitive inhibitor of sarco/ER Ca(2+)-ATPase, thapsigargin.

17 s store-operated Ca(2+) influx stimulated by thapsigargin.

18 C but was partially blocked by ryanodine or thapsigargin.

19 vement of these cells in the biosynthesis of thapsigargin.

20 ) store depletion, using ATP (100 microM) or thapsigargin (1 microM), revealed greater relative store

21 ects on membrane potential, was inhibited by thapsigargin (1 muM) or the L-type Ca(2+) channel blocke

22 Brief application of thapsigargin (1 mum) resulted in a decrease of SERCA act

23 which was amplified by store depletion with thapsigargin (1 mum), and was significantly reduced by b

24 plasmic reticulum with ryanodine (2 mum) and thapsigargin (1 mum).

25 high concentrations of FCCP (100 microM) and thapsigargin (10 microM) indicating that they originated

26 In contrast, flecainide (10 muM) and thapsigargin (10 muM) eliminated all afterdepolarization

27 epletion of intracellular Ca(2+) stores with thapsigargin (10 mum), inhibition of casein kinase 2 (4,

28 luo-5N) after complete SERCA inhibition with thapsigargin (10 mum).

29 oxic as compared to the natural product lead thapsigargin 2.

30 Depleting SR Ca(2+) using thapsigargin (2-10 microM) changed neither the STIM1 dis

31 nd endoplasmic reticulum (ER) stress inducer thapsigargin (25 nM) or tunicamycin (3 or 10 microM).

32 tress inducers tunicamycin (3 or 10 muM) and thapsigargin (25 or 100 nM) for 6 hours or longer.

33 eir corresponding redox derivatives, such as thapsigargin, a cytotoxic natural product with potent an

34 pressing either T4 or T4C3 were treated with thapsigargin, a drug, which has been shown to induce end

35 Accordingly, thapsigargin, a known ER stress inducer, stimulated ET-1

36 Thapsigargin, a sarco/endoplasmic reticulum Ca(2+)-ATPas

37 LPS-stimulated macrophages incubated with thapsigargin, a sarcoplasmic/endoplasmic reticulum calci

38 (-/-) mouse embryonic fibroblasts exposed to thapsigargin, A23187, brefeldin A, DTT, geldanamycin, or

39 dine) and SERCA pump (cyclopiazonic acid and thapsigargin) abolished Ca(2+) transients elicited by pu

40 Exposure to thapsigargin accelerates DeltaPsi loss and apoptosis of

41 ic reticulum Ca(2+)-ATPase (SERCA) inhibitor thapsigargin, accompanied by similar kinetics and intens

42 lasmic reticulum distribution and revealed a thapsigargin-activated I(SOC) that was abolished by noco

43 Whereas thapsigargin activates the I(SOC) in pulmonary artery en

44 Thapsigargin also elicited a small decrease in PLB-SERCA

45 In addition, topical thapsigargin also increases production of the murine hom

46 The SERCA inhibitor thapsigargin also stimulates phosphorylation of both bet

47 Induction of ER stress by thapsigargin also up-regulated IL-23p19 in primary B lym

48 (C2Cer), which increases S1P production, or thapsigargin (an ER stressor), applied to cultured human

49 We report that thapsigargin, an ER stressor widely used to induce autop

50 ith lactacystin, a proteasome inhibitor, and thapsigargin, an inducer of endoplasmic reticulum stress

51 Thapsigargin, an inducer of the UPR that does not interf

52 +) from the endoplasmic reticulum induced by thapsigargin, an inhibitor of endoplasmic reticulum Ca(2

53 ignaling of NRR mutants, augmented effect of Thapsigargin, an inhibitor of mutant Notch1, but had no

54 f-life approximately 37 min) was enhanced by thapsigargin, an inhibitor of the endoplasmic calcium-AT

55 ce of the permeability wave was inhibited by thapsigargin, an inhibitor of the endoplasmic reticulum

56 , rats infused in the dorsal CA1 region with thapsigargin, an irreversible inhibitor of the SERCA pum

57 Both thapsigargin and A23187 stimulated robust [(3)H]arachido

58 Recovery from cellular stresses such as thapsigargin and ATP depletion induced increased express

59 Ryanodine-thapsigargin and caffeine protected against nsPEF-induce

60 epletion of intracellular Ca(2+) stores with thapsigargin and caffeine, or buffering of intracellular

61 The ER stress inducers thapsigargin and dithiothreitol trigger production of th

62 In the presence of thapsigargin and external calcium, the levels of the mRN

63 stress-induced rise in [Ca(2+)](i), whereas thapsigargin and extracellular Ca(2+) depletion together

64 ering endoplasmic reticulum (ER) stress with thapsigargin and in islets of ob/ob mice.

65 M1 in H123 cells rescued SOCE in response to thapsigargin and ionomycin and abrogated IFN-alpha/beta-

66 taurolithocholate, or Ca(2+) mobilization by thapsigargin and ionomycin.

67 LA(2)beta is responsible for the majority of thapsigargin and ionophore (A23187)-induced arachidonic

68 concise, efficient and scalable synthesis of thapsigargin and nortrilobolide from commercially availa

69 d protein trafficking and folding induced by thapsigargin and palmitate.

70 sabling the sarcoplasmic reticulum (SR) with thapsigargin and ryanodine.

71 a(2+) signals were influenced in response to thapsigargin and sequential treatment with acetylcholine

72 Thapsigargin and sodium 4-phenyl butyrate were inefficie

73 Their responses to thapsigargin and t-butyl hydroperoxide-induced cell deat

74 n extensive hydrogen-bonding network between thapsigargin and the backbone of SERCA.

75 utant neuronal cells to apoptosis induced by thapsigargin and the mutant laforin proteins.

76 However, when Hrd1 was knocked down, thapsigargin and tunicamycin dramatically decreased ERAD

77 In cardiac myocytes, the ER stressors, thapsigargin and tunicamycin increased ERAD, as well as

78 muscle with endoplasmic reticulum stressors thapsigargin and tunicamycin increases tribbles 3 and im

79 cell death caused by inducers of ER stress (thapsigargin and tunicamycin) but not by inducers of ext

80 ation, TNF and cycloheximide, staurosporine, thapsigargin and tunicamycin).

81 n, and suppressed cell death induced by both thapsigargin and tunicamycin, two drugs that induce ER s

82 ble complex that is highly resistant to both thapsigargin and vanadate.

83 nvestigated using the Ca(2+)-pump inhibitors thapsigargin and vanadate.

84 g normal regulation of cross-linking by ATP, thapsigargin, and anti-PLB antibody.

85 iet-induced obese rats and rats administered thapsigargin, and by combining metabolic, histologic, ph

86 esponse to tunicamycin, brefeldin A (brefA), thapsigargin, and DTT that lead to accumulation of unfol

87 ter apoptosis when treated with tunicamycin, thapsigargin, and l-Hcy, compared with CSE(+/+) MEFs.

88 l death, including ER stressors tunicamycin, thapsigargin, and physiological concentrations of palmit

89 urons when stores were maximally depleted by thapsigargin, and STIM1 and Orai1 levels were not altere

90 e chemotherapeutic agents VP-16, paclitaxel, thapsigargin, and temozolomide.

91 ntracellular Ca(2+) chelation, aggravated by thapsigargin, and unaffected by removal of extracellular

92 mic reticulum (ER) stressors and can prevent thapsigargin- and palmitate-induced dysfunction and cell

93 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, m

94 parietal cells, we showed that gadolinium-, thapsigargin-, and carbachol-mediated release of Ca(2+)(

95 Accordingly, we found that the UPR agonist thapsigargin attenuated mutant Smoothened-induced phenot

96 was blocked with the Ca(2+)-ATPase inhibitor thapsigargin, bax-deficient neurons showed strongly elev

97 Here, we present the putative second step in thapsigargin biosynthesis, by showing that the cytochrom

98 s study paves the way for further studies of thapsigargin biosynthesis.

99 quired for complete autophagy flux, and that thapsigargin blocks recruitment of Rab7 to autophagosome

100 Thapsigargin blocks the sarco/endoplasmic Ca(2+) ATPase

101 horylation, an increase in [Ca(2+)](i) using thapsigargin, bradykinin, or acetylcholine can increase

102 m stores, an effect that could be blocked by thapsigargin but not by EGTA.

103 Nuli-1 cells pretreated with thapsigargin but not calcium ionophore exhibited increas

104 ed the cytotoxic effects of flavopiridol and thapsigargin, but not the other agents.

105 cells following induction of ER stress with thapsigargin, but only caspase-3 cleavage is amplified i

106 um calcium ATPase with cyclopiazonic acid or thapsigargin), Ca(2+) waves ceased to occur at a [Ca(2+)

107 On perfusion with thapsigargin, Ca(2+) transient amplitude and cell shorte

108 Moreover, direct induction of ER stress with thapsigargin caused a similar decrease in stemness and s

109 Thapsigargin caused progressive loss of [Ca(2+)](ne/er),

110 Following long-term treatment with thapsigargin, cells expressing T4C3 presented with a mar

111 augmented by ATP but abolished by Ca(2+) or thapsigargin, confirming in native SR vesicles that PLB

112 tect beta-cells against ER stress induced by thapsigargin, cyclopiazonic acid, palmitate, insulin ove

113 Heart rate did not change, although thapsigargin decreased left ventricular systolic functio

114 atinocytes treated with the SERCA2-inhibitor thapsigargin, depletes ER Ca2+ stores, leading to consti

115 duced elevation of [Ca(2+)](ne/er) following thapsigargin depletion occurred in cells containing litt

116 ar Ca(2+) stores by the SERCA pump inhibitor thapsigargin, depolarization-induced constrictions in MV

117 Remarkably, thapsigargin did not inhibit bulk DNA synthesis or activ

118 fat diet or that were centrally administered thapsigargin displayed hypothalamic ER stress, whereas g

119 Thapsigargin does not affect autophagosome formation but

120 Furthermore, when exposed to thapsigargin, dwarf fibroblasts display attenuated splic

121 U73112 or depleting ER Ca(2+) with prolonged thapsigargin/EGTA treatment.

122 Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRN

123 t of staurosporine (mitochondrial damage) or thapsigargin (ER stress).

124 d neurite structures and ER store depletion (thapsigargin) evoked Ca(2+) transients from these struct

125 pite this physical association, we find that thapsigargin fails to activate SOCE following coexpressi

126 Similar to thapsigargin, flavopiridol robustly induces a distinct p

127 phodiesterase inhibitor, rolipram, prevented thapsigargin from inducing perivascular cuffs and decrea

128 eatment with a panel of chemical chaperones (thapsigargin, glycerol or sodium 4-phenylbutyrate), we d

129 ile the internal Ca2+ stores depleting agent thapsigargin had negligible effect.

130 si m) and weak caspase-9 activation, whereas thapsigargin had no effect.

131 Strikingly, thapsigargin has no effect on endocytosis-mediated degra

132 beta-catenin translocation are suppressed by thapsigargin in PC3 cell line.

133 SR)) after complete inhibition of SERCA with thapsigargin in permeabilized rabbit ventricular myocyte

134 Knowledge of thapsigargin in planta storage and biosynthesis has been

135 lecules are present in the binding cavity of thapsigargin in sarco/endoplasmic reticulum calcium ATPa

136 TRPC4 exaggerated permeability responses to thapsigargin in Sugen/hypoxia-treated PAH rats.

137 Pase pumps in the endoplasmic reticulum with thapsigargin in the absence of external Ca(2+).

138 in the plasma membrane region of cells, and thapsigargin increased co-immunoprecipitation of TRPC1 w

139 ndoplasmic reticulum stress, tunicamycin and thapsigargin, increased TRB3 levels in normal cells.

140 1 in spe-38 mutant spermatozoa, ionomycin or thapsigargin induced influx of Ca(2+) remains unperturbe

141 ns that cause ER Ca(2+) depletion, including thapsigargin, induced SREBP2-dependent up-regulation of

142 s-inducing agents, including tunicamycin and thapsigargin, induced the expression of CSE in ATF4(+/+)

143 We show that both thapsigargin-induced and spontaneous ER stress are assoc

144 al and proliferation and protected them from thapsigargin-induced apoptosis (P<.0001) in vitro.

145 ans in Bok(-/-) mice exhibited resistance to thapsigargin-induced apoptosis in vivo.

146 ion of TCTP partially protects cells against thapsigargin-induced apoptosis, as measured using caspas

147 transfected with hRes showed protection from thapsigargin-induced apoptosis.

148 Thapsigargin-induced beta-cell apoptosis and ceramide ge

149 not effectively protect against palmitate or thapsigargin-induced beta-cell apoptosis, but specifical

150 difficile toxin B, which we find to inhibit thapsigargin-induced beta-cell p38 MAPK phosphorylation.

151 nhibitors of store-operated channels blocked thapsigargin-induced Ca(2+) entry but only partially red

152 current in rat basophilic leukemia cells and thapsigargin-induced Ca(2+) influx in Jurkat T cells.

153 increased both the rate and magnitude of the thapsigargin-induced Ca(2+) transient suggesting that Ca

154 Thus, Orai-1, -2, and -3 enhanced thapsigargin-induced calcium entry by 50-150% in cells s

155 ion had no significant effect on endogenous, thapsigargin-induced calcium entry in wild-type cells (H

156 down of STIM1 or Orai1 substantially reduced thapsigargin-induced calcium entry, and more modestly di

157 3 decreased serum deprivation, cytokine, and thapsigargin-induced cell death under hyperglycemic cond

158 ounds that rescued a neuronal cell line from thapsigargin-induced cell death, we identified benzodiaz

159 estration of membrane cholesterol attenuated thapsigargin-induced clustering of STIM1 as well as SOCE

160 m (SER), predispose Purkinje neurons (PN) to thapsigargin-induced endoplasmic reticulum (ER) stress.

161 that SEC62 silencing sensitized the cells to thapsigargin-induced endoplasmic reticulum stress.

162 With bovine endothelial cells, thapsigargin-induced ER Ca(2+) release caused a dose-dep

163 etabolism by cyclooxygenases, in response to thapsigargin-induced ER stress as compared with control

164 In this study, we found that thapsigargin-induced ER stress augmented recruitment of

165 and human beta-cells exposed to cytokines or thapsigargin-induced ER stress.

166 the EF and PF groups supports the finding of thapsigargin-induced ER stress.

167 intracellular Ca(2+) by treating cells with thapsigargin induces diacylglycerol production at the Go

168 Here we show that thapsigargin induces higher expression of CHOP, enhanced

169 compliance dose-dependently decreased after thapsigargin infusion, attributable to an increase in ti

170 doplasmic reticulum Ca(2+) ATPase) inhibitor thapsigargin inhibits mutant NOTCH1 receptors compared w

171 logic model that delivered ER stress inducer thapsigargin into the brain, this study demonstrated tha

172 Furthermore, we show that thapsigargin is likely to be stored in secretory ducts i

173 ponse to Ag or the calcium mobilizing agent, thapsigargin, is dependent on emptying of intracellular

174 A, whereas acute ER stress caused by DTT and thapsigargin leads to rapid and specific degradation of

175 onged exposure of beta-cells to cytokines or thapsigargin leads to THBS1 and MANF degradation and los

176 of cells with the non-genotoxic UPR agonist thapsigargin led to a rapid inhibition of DNA synthesis

177 Confocal microscopy shows that thapsigargin-mediated depletion of ER Ca(2+) stores in R

178 Similarly, thapsigargin-mediated endoplasmic reticulum (ER) Ca(2+)

179 neuronal susceptibility to both hypoxic and thapsigargin-mediated injury and attenuated brain-derive

180 The orientation of the thapsigargin molecule in SERCA is crucially dependent on

181 er affinities, severalfold greater than even thapsigargin (nanomolar or higher).

182 The effects of thapsigargin on EBV lytic gene expression are also inhib

183 Effects of tunicamycin and thapsigargin on IL-1beta- and TNF-alpha-stimulated MCP-1

184 hyl sulfoxide), and the Ca(2+)-ATP inhibitor thapsigargin only slightly relieved ER retention and inc

185 annels are activated by STIM1 in response to thapsigargin or ACh.

186 Cerebellar slices were treated with thapsigargin or as controls for three hours in oxygenate

187 ER depletion in vagal sensory neurons (using thapsigargin or caffeine) in the absence of extracellula

188 Here we report that treatment with thapsigargin or cellular agonists results in association

189 essors tunicamycin and HIV-1 Tat, but not to thapsigargin or dithiothreitol.

190 g exposure to these two agonists, but not to thapsigargin or dithiothreitol.

191 n calcium, and the depletion of calcium with thapsigargin or ethylene glycol tetraacetic acid (EGTA)

192 Thapsigargin or extracellular Ca(2+) depletion partially

193 -1 on caspase-dependent apoptosis induced by thapsigargin or glucose deprivation in INS-1 beta-cells.

194 tolbutamide or gliclazide were inhibited by thapsigargin or nicardipine and were significantly poten

195 ere, we show that passive store depletion by thapsigargin or receptor activation by either thrombin o

196 + (SOC) entry because SOC entry induced with thapsigargin or small interfering RNA-mediated inhibitio

197 Here, we report that ER stressors, such as thapsigargin or the clinically used proteasome inhibitor

198 uction of ER stress by treatment with either thapsigargin or tunicamycin activated autophagy in immor

199 here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblas

200 pidium iodide-positive nuclei in response to thapsigargin or tunicamycin treatment.

201 ically different, pharmacological stressors, thapsigargin or tunicamycin.

202 R stress responses triggered by ER-stressors thapsigargin or tunicamycin.

203 cium transients and reduced AA release after thapsigargin or UTP treatment with decreased ERK1/2 and

204 a unique E2.ATP state that is unable to bind thapsigargin or vanadate.

205 s (TRAP, thrombin, convulxin, collagen, PMA, thapsigargin, or A23187) and all led to a time-dependent

206 on of endoplasmic reticulum Ca(2+) stores by thapsigargin, or blockade of Ca(2+) release from these s

207 y reduced by extracellular Ca(2+) depletion, thapsigargin, or Ca(V)1.3 knockdown.

208 or without treatment with 17beta-estradiol, thapsigargin, or G-1.

209 nduction of protein misfolding by puromycin, thapsigargin, or geldanamycin resulted in inflammasome a

210 cue by low temperature, chemical correctors, thapsigargin, or overexpression of GRASP55, DeltaF508CFT

211 Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same

212 After SMCs were exposed to A23187, thapsigargin, or tunicamycin, intracellular calcium leve

213 senite-induced oxidative stress differs from thapsigargin- or tunicamycin-induced ER stress in promot

214 h other toxic stimuli such as staurosporine, thapsigargin, paraquat, and H(2)O(2) showed significantl

215 reticulum Ca2+ depletion with ryanodine and thapsigargin prevented isoproterenol-induced LDCAE and b

216 ther enhanced in combination with a targeted thapsigargin prodrug (G202) that selectively kills tumor

217 Thapsigargin produced perivascular fluid cuffs along ext

218 m trasport ATPase (SERCA) pump activity with thapsigargin prolonged NMDAR-DeltaCa(2+) responses in MN

219 the ER sarco/ER Ca(2+)-ATPase pump inhibitor thapsigargin rescues the calcium influx defect in Atg7-d

220 In each case thapsigargin-resistant DNA synthesis was due to an incre

221 Treatment of mutant cells with thapsigargin resulted in a significant decrease in mitoc

222 Passive depletion of ER Ca(2+) stores with thapsigargin resulted in a significant raise in [Ca(2+)]

223 cell lines with fenretinide, bortezomib, or thapsigargin resulted in induction of eIF2alpha signalin

224 Treatment of U937 cells with tunicamycin/thapsigargin resulted in reduced hRes secretion and conc

225 activation of Icrac without interfering with thapsigargin-sensitive Ca(2+) store release.

226 namide mononucleotide, the Ca(2+) content of thapsigargin-sensitive Ca(2+) stores as well as cell res

227 Accordingly, the Ca(2+) content of thapsigargin-sensitive Ca(2+) stores was greatly reduced

228 by mobilization of intracellular Ca(2+) from thapsigargin-sensitive Ca(2+) stores.

229 HNO increased the maximal rate of thapsigargin-sensitive Ca2+ uptake mediated by SERCA in

230 lease activated current), as well as a large thapsigargin-sensitive inward current activated by withd

231 ellular calcium levels required release from thapsigargin-sensitive stores by a pertussis toxin-insen

232 s (HEK-293, COS1), in HEK cells expressing a thapsigargin-sensitive variant of TRPC3 (TRPC3a), or in

233 The mechanism of thapsigargin sensitivity was Ca(2+)-mediated, and autoph

234 The discharge of intracellular stores with thapsigargin stimulated mTORC1 activity (measured as S6

235 epletion triggered by acetylcholine (ACh) or thapsigargin stimulated the formation of a ternary compl

236 CK1-IP(3)R association without any change in thapsigargin-stimulated Ca(2+) release and entry.

237 We found that thapsigargin-stimulated Ca(2+) signals were increased in

238 ate reader intracellular Ca(2+) assays using thapsigargin-stimulated Jurkat T cells and its detailed

239 Thapsigargin stimulation of cells expressing Orai1+STIM1

240 Thapsigargin stimulation of cells expressing TRPC1+STIM1

241 ulation for Ca(2+) entry was confirmed using thapsigargin studies.

242 nity of the PLB-SERCA complex with Ca(2+) or thapsigargin suggests that the binding interface is alte

243 Thapsigargin (Tg) blocks the sarco/endoplasmic reticulum

244 hat serotonin (5-HT) or store depletion with thapsigargin (TG) enhanced intracellular free Ca(2+) con

245 e exposure to the chemical ER-stress inducer thapsigargin (TG) followed by recovery resulted in the a

246 n of endoplasmic reticulum stress (ERS) with thapsigargin (TG) increased SGK1 mRNA and protein expres

247 SERCA2b with the specific SERCA2 inhibitors thapsigargin (TG) or small interfering RNA to SERCA2b.

248 transmission we applied tunicamycin (TM) or thapsigargin (TG) to hippocampal neurons, which triggere

249 ions of the commonly used SERCA1a inhibitors thapsigargin (Tg), cyclopiazonic acid, and 2,5-di-tert-b

250 imulated with a pharmacological ER stressor, thapsigargin (Tg), increased hBD2/hBD3 as well as CAMP m

251 ven AML cells through a similar mechanism as thapsigargin (TG), involving increased cytosolic calcium

252 calcium stores by calcium mobilizers such as thapsigargin (TG), resulting in preparation (priming) of

253 ch as the ER-Ca(2+)-ATPase (SERCA) inhibitor thapsigargin (TG).

254 ion but not store depletion, induced here by thapsigargin (TG).

255 ndoplasmic reticulum Ca(2+)-ATPase inhibitor thapsigargin (TG).

256 acrophages with the ER stress-inducing agent thapsigargin (TG; 1 muM) increasedL.

257 acrophages with the ER stress-inducing agent thapsigargin (TG; 1 muM) increasedL.amazonensisinfectivi

258 ndoplasmic reticulum (ER) stressors, such as thapsigargin, than cells from normal mice.

259 ells incubated with insulin secretagogues or thapsigargin, that this requires prior iPLA(2)beta activ

260 ase activity was irreversibly inhibited with thapsigargin, the S170F and DeltaE9 cells showed larger

261 n of CRT, BiP, gp96, and PDI were induced by thapsigargin (THP) treatment, which depletes ER calcium,

262 conditions and also following challenge with thapsigargin (THPS), an inhibitor of sarco/endoplasmic r

263 ls or murine primary enamel organ cells with thapsigargin to activate SOCE leads to increased express

264 parasite were selectively discharged, using thapsigargin to deplete endoplasmic reticulum (ER) Ca(2+

265 bitors, phorbol 12-myristate 13-acetate, and thapsigargin to modulate [Ca(2+)](i) implicated conventi

266 stimulated by either a calcium ionophore or thapsigargin to produce NO.

267 uding Ser-1179 or Thr-497, was unaffected in thapsigargin-treated cells.

268 nd reduced cell viability in lactacystin and thapsigargin-treated cells.

269 sistent with this possibility, incubation of thapsigargin-treated INS-1 beta cells with the PPAR-gamm

270 liminated, while unloading of Ca2+ stores by thapsigargin treatment in the absence of extracellular C

271 We also found that thapsigargin treatment of A20 lymphoma cells up-regulate

272 Thapsigargin treatment of beta cells in vitro induces a

273 Thapsigargin treatment of T4 or T4C3 cells, which causes

274 alcium levels and intracellular CRT, because thapsigargin treatment reduced collagen expression, wher

275 itions and were increased by lactacystin and thapsigargin treatment, and growth of L110R MM-1alpha ce

276 ntent and release, whether experimentally by thapsigargin treatment, or in the model, desynchronized

277 ylation due to calcium-mobilizing ER stress (thapsigargin treatment, oxygen-glucose deprivation) crit

278 stinfection compared with mock infection and thapsigargin treatment.

279 ated in MM cells during ER stress induced by thapsigargin, tunicamycin or the myeloma therapeutic bor

280 Thapsigargin up-regulated heat-shock proteins (HSPs) and

281 onjugated folate to an alcohol derivative of thapsigargin via a cleavable ester linkage.

282 cing the UPR by creating mild ER stress with thapsigargin was able to reverse the defect in myoblast

283 uced Ca(2+) release that were prevented when thapsigargin was added to predeplete the SR or by mitoch

284 ion in healthy control PBMCs stimulated with thapsigargin was analyzed by DNA microarray.

285 Thapsigargin was infused into a central venous catheter

286 ry Ca2+ response, but when xestospongin C or thapsigargin was loaded into ECs and BAPTA into VSMCs, i

287 h in response to fenretinide, bortezomib, or thapsigargin was not abrogated by inhibition of eIF2alph

288 To test this hypothesis, the plant alkaloid thapsigargin was used to activate store-operated calcium

289 10, the ER stress activators tunicamycin and thapsigargin were even more potent enhancers of hRPE cas

290 gical inducers of ER stress, tunicamycin and thapsigargin, were found to increase the expression of p

291 and lysophosphatidic acid but not by fMLP or thapsigargin, whereas 13'-carboxychromanol decreased cel

292 Stimulation of degranulation by thapsigargin, which bypasses inositol 1,4,5-trisphosphat

293 However, in cells treated with thapsigargin, which depletes endoplasmic reticulum calci

294 ltage-dependent Ca(2+) channel inhibitor, or thapsigargin, which depletes intracellular Ca(2+) stores

295 The spine expansion was suppressed by thapsigargin, which disables calcium stores.

296 lide (Tb) is a potent natural counterpart of thapsigargin, which has shown promising results in cance

297 protein-coupled receptor ligand, C3a, or by thapsigargin, which induces a receptor-independent calci

298 In fibroblasts stimulated with thapsigargin, which induces MPTP formation by a direct e

299 Topical application of thapsigargin, which inhibits the ER Ca(2+) ATPase activi

300 ltiple calcium-elevating agonists, including thapsigargin, without inhibition of calcium elevation, c