ライフサイエンスコーパス: thapsigargin

1 ctile activity was not further diminished by thapsigargin.

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

3 C but was partially blocked by ryanodine or thapsigargin.

4 e sensitivity of HAECs to both histamine and thapsigargin.

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

6 the cell death caused by the SERCA inhibitor thapsigargin.

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

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

9 GRP94, and ERp72 proteins after exposure to thapsigargin.

10 mical inducers of ER stress, tunicamycin and thapsigargin.

11 icular end diastolic pressure was altered by thapsigargin.

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

13 anced activation of the UPR upon exposure to thapsigargin.

14 lcium stores, as indicated by depletion with thapsigargin.

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

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

17 ncreased sensitivity to apoptosis induced by thapsigargin.

18 vement of these cells in the biosynthesis of thapsigargin.

19 ndoplasmic reticulum Ca-ATPase activity with thapsigargin.

20 y carrot, produces the highly toxic compound thapsigargin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 roach toward the [5-7]fused bicyclic core of thapsigargin, a subnanomolar inhibitor of the endo/sarco

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

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

43 Exposure to thapsigargin accelerates DeltaPsi loss and apoptosis of

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

45 Thapsigargin also elicited a small decrease in PLB-SERCA

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

47 The SERCA inhibitor thapsigargin also stimulates phosphorylation of both bet

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

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

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

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

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

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

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

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

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

57 endoplasmic reticulum (ER) stress induced by thapsigargin, an inhibitor of the sarcoplasmic or endopl

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

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

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

61 Ryanodine-thapsigargin and caffeine protected against nsPEF-induce

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

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

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

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

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

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

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

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

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

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

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

75 We show that thapsigargin and thrombin-induced SOCE was markedly redu

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

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

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

93 These profound differences between thapsigargin- and tunicamycin-treated cells upon inflamm

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

95 However, the effect was specific to thapsigargin, as tunicamycin and the subtilase cytotoxin

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

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

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

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

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

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

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

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

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

105 ve to Salmonella infection when treated with thapsigargin but not with tunicamycin.

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

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

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

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

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

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

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

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

114 Our results suggest that Thapsigargin could be repurposed to tackle S. aureus hos

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

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

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

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

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

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

121 w that cells undergoing ER stress induced by thapsigargin display a significant increase in NF-kappaB

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

123 ls treated with ER stress inducers including thapsigargin, dithiothreitol, and NGI-1.

124 Thapsigargin does not affect autophagosome formation but

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

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

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

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

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

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

131 Similar to thapsigargin, flavopiridol robustly induces a distinct p

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

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

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

135 pumps and treatment with the SERCA-inhibitor Thapsigargin halted intracellular MRSA survival.

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

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

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

139 Knowledge of thapsigargin in planta storage and biosynthesis has been

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

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

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

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

144 1 in spe-38 mutant spermatozoa, ionomycin or thapsigargin induced influx of Ca(2+) remains unperturbe

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

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

147 lular and extracellular calcium in mediating thapsigargin-induced and NOD-dependent pro-inflammatory

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

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

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

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

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

153 Thapsigargin-induced beta-cell apoptosis and ceramide ge

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

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

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

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

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

159 3 decreased serum deprivation, cytokine, and thapsigargin-induced cell death under hyperglycemic cond

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

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

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

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

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

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

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

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

168 As lowered ER stress in NOD mice, suppressed thapsigargin-induced PARP cleavage in human islets, and

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

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

171 Here, we confirm that thapsigargin induces NOD-dependent pro-inflammatory sign

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

173 Reciprocally, thapsigargin inhibition of a fraction of the population

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

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

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

177 e, a derivative of the sesquiterpene lactone thapsigargin, is gradually approaching a clinical applic

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

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

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

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

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

183 not from nonreductive ER stresses caused by thapsigargin-mediated ER Ca(2+) depletion or tunicamycin

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

185 to the cell culture medium were required for thapsigargin-mediated NOD activation.

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

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

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

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

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

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

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

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

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

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

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

197 Thapsigargin or extracellular Ca(2+) depletion partially

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

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

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

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

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

203 ically different, pharmacological stressors, thapsigargin or tunicamycin.

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

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

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

207 cking Ca(2+) release with a SERCA inhibitor (thapsigargin) or a store-operated Ca(2+) entry blocker (

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

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

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

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

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

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

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

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

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

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

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

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

220 Thapsigargin produced perivascular fluid cuffs along ext

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

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

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

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

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

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

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

228 taining and Ca(++)-free solutions containing thapsigargin, ryanodine, BAPTA-AM, 18-alpha-glycyrrhetin

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

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

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

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

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

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

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

236 Results demonstrated that SERCA inhibitor, thapsigargin, significantly reduced lymphatic phasic con

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

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

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

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

241 Thapsigargin stimulation of cells expressing Orai1+STIM1

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 intracellular free Ca(2+), its responses to thapsigargin (TG), an ER Ca(2+)-ATPase blocker, and stor

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

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

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

253 impairs secretion of destabilized TTR during thapsigargin (Tg)-induced ER stress by increasing its ER

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

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

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

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

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

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

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

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

262 -ATPase pumps, cyclopiazonic acid (CPA), and thapsigargin (Thg).

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

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

265 t two distinct ER stressors, tunicamycin and thapsigargin, through activation of the JAK2/STAT5 pathw

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

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

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

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

270 artemisinin (ART, 1), parthenolide (PTL, 2), thapsigargin (TPG, 3), andrographolide (AGL, 4), ginkgol

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

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

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

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

275 Thapsigargin treatment of beta cells in vitro induces a

276 Thapsigargin treatment of T4 or T4C3 cells, which causes

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

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

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

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

281 stinfection compared with mock infection and thapsigargin treatment.

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

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

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

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

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

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

288 Thapsigargin was infused into a central venous catheter

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

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

291 10, the ER stress activators tunicamycin and thapsigargin were even more potent enhancers of hRPE cas

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

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

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

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

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

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

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

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

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

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