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1 sceptibility to unrelated inhibitors such as cyclopiazonic acid.
2 rcoplasmic reticulum (SR) with ryanodine and cyclopiazonic acid.
3 e L263E mutation is also more susceptible to cyclopiazonic acid.
4 luorescein isothiocyanate, thapsigargin, and cyclopiazonic acid.
5 tiated Ca2+ entry with low concentrations of cyclopiazonic acid.
6 plasmic reticulum (ER) sequestration blocker cyclopiazonic acid.
7 shed by cotreatment with the SERCA inhibitor cyclopiazonic acid.
8 ically dimethylallylates cAATrp to form beta-cyclopiazonic acid.
9 an twofold after depletion by treatment with cyclopiazonic acid.
10 ic acid; m/z 357/210 and 357/191 for (13)C20-cyclopiazonic acid.
11 nodine, 0.1 microM thapsigargin or 10 microM cyclopiazonic acid.
12 cells treated with a SR Ca2+-pump inhibitor, cyclopiazonic acid.
13 of endoplasmic reticulum Ca(2+)-ATPase pump, cyclopiazonic acid.
16 Similar hyperpolarization was evoked with cyclopiazonic acid (10 microM, an inhibitor of sarcoplas
20 Caffeine (10 mM), ryanodine (10 microM), cyclopiazonic acid (30 microM) or CCCP (10 microM) had n
22 /endoplasmic reticulum Ca2+-ATPase inhibitor cyclopiazonic acid (30 mum) was also applied during the
24 lum Ca2+ release with Ca2+-ATPase inhibitors cyclopiazonic acid (5 microM) or thapsigargin (5 microM)
25 (5 micromol/L), ryanodine (5 micromol/L), or cyclopiazonic acid (5 micromol/L) in Ca2+-containing or
27 , a selective blocker of Ca2+ release and by cyclopiazonic acid, a blocker of Ca2+ sequestration into
28 r application of thapsigargin, ryanodine, or cyclopiazonic acid, a hypoxic challenge produced no furt
29 entry (SOCE) by passive store depletion with cyclopiazonic acid, a reversible blocker of sarco-endopl
31 pletion of intracellular Ca(2+) stores using cyclopiazonic acid abolished SAH-induced eHACSs and rest
32 evious depletion of the ER calcium stores by cyclopiazonic acid abolished the HP-induced calcium leve
33 f the sarcoplasmic reticulum Ca2+ pump (with cyclopiazonic acid) abolished Ca2+ oscillations in all c
36 on of endoplasmic reticular Ca2+ uptake with cyclopiazonic acid also had little effect on stimulation
37 2+ stores by perifusion with thapsigargin or cyclopiazonic acid also reduced DAP amplitudes by approx
39 lowed in the presence of either ryanodine or cyclopiazonic acid (an inhibitor of the SR Ca2+-ATPase).
40 Ca(2+), depletion of ER Ca(2+) stores using cyclopiazonic acid, an ER Ca(2+)-ATPase inhibitor, and c
41 ent increase in [Ca2+]in that was blocked by cyclopiazonic acid, an inhibitor of endoplasmic reticulu
42 ined by a short treatment with 2.5-10 microm cyclopiazonic acid, an inhibitor of the sarco/endoplasmi
43 Two structurally distinct SERCA inhibitors, cyclopiazonic acid and 2,5-di-[t-butyl]-1,4-hydroquinone
45 ere ablated by inhibiting Ca(2+) stores with cyclopiazonic acid and reduced by inhibiting Ca(2+) infl
47 nodine receptors (Ryanodine) and SERCA pump (cyclopiazonic acid and thapsigargin) abolished Ca(2+) tr
48 ndoplasmic reticulum Ca(2+)-ATPase inhibitor cyclopiazonic acid and was attenuated by pre-incubation
50 y to inhibitors (vanadate, thapsigargin, and cyclopiazonic acid) and affinity for substrates (MgATP a
51 m Ca2+-transporting ATPase (SERCA; 10 microM cyclopiazonic acid) and/or sarcolemmal Na+-Ca2+ exchange
52 y used SERCA1a inhibitors thapsigargin (Tg), cyclopiazonic acid, and 2,5-di-tert-butylhydroquinone.
53 ,N',N'-tetraacetic acid acetoxymethyl ester, cyclopiazonic acid, and N,N,N',N'-tetrakis(2-pyridylmeth
54 doplasmic reticulum Ca2+ pump (thapsigargin, cyclopiazonic acid, and tert-butylhydroquinone), and pro
55 ndoplasmic reticulum calcium ATPase (SERCA), cyclopiazonic acid, and thapsigargin (1) selectively enh
58 Depleting intracellular Ca(2+) stores with cyclopiazonic acid completely blocked both the outward c
59 (caffeine) and SR calcium-ATPase inhibitor (cyclopiazonic acid), consistent with studies suggesting
62 intracellular Ca(2+) store-depleting agents cyclopiazonic acid (CPA) and 1,2-bis-(2-aminophenoxy)eth
65 ry cultured mouse PASMCs loaded with fura-2, cyclopiazonic acid (CPA) caused a transient followed by
66 We extend the latter hypothesis employing cyclopiazonic acid (CPA) challenge, which similarly incr
67 in slices, we found that SERCA inhibition by cyclopiazonic acid (CPA) decreased evoked [DA](o) in the
68 smic reticulum Ca2+-ATPase (SERCA) inhibitor cyclopiazonic acid (CPA) dramatically affected oscillati
70 to NO were inhibited by thapsigargin (TG) or cyclopiazonic acid (CPA) indicating the involvement of s
75 (2+) in living normal rat kidney cells using cyclopiazonic acid (CPA) resulted in the extreme expansi
77 Ca2+ by inhibiting the SR Ca2+-ATPase (with cyclopiazonic acid (CPA), 20 microM) resulted in an enha
80 ed skeletal muscle cells were depleted using cyclopiazonic acid (CPA), a reversible inhibitor of Ca2+
81 A slow decline of tension was produced by cyclopiazonic acid (CPA), a sarcoplasmic reticulum Ca2+
82 ion following stimulation in the presence of cyclopiazonic acid (CPA), a sarcoplasmic reticulum Ca2+-
84 ted sarcoplasmic reticulum Ca2+ pumping with cyclopiazonic acid (CPA), an inhibitor of the sarco(endo
98 eceptors (RyRs), or thapsigargin (500 nM) or cyclopiazonic acid (CPA, 10 microM), to inhibit the SR C
99 s were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20-40 microM), a blocker of Ca2
101 t isoprenaline reduced the current evoked by cyclopiazonic acid (CPA, sarcoplasmic/endoplasmic reticu
113 tions were used: m/z 337/196 and 337/182 for cyclopiazonic acid; m/z 357/210 and 357/191 for (13)C20-
117 2+ uptake by the sarcoplasmic reticulum with cyclopiazonic acid or thapsigargin did not prevent accel
118 ic/endoplasmic reticulum calcium ATPase with cyclopiazonic acid or thapsigargin), Ca(2+) waves ceased
119 s against ER stress induced by thapsigargin, cyclopiazonic acid, palmitate, insulin overexpression, a
120 (3 nm) pre-incubation also augmented 10 muM cyclopiazonic acid plus 10 mm caffeine-evoked release of
122 to Ca(2+) mobilizers such as thapsigargin or cyclopiazonic acid primes the releasable pool of vasopre
123 RCA blockers thapsigargin, thapsigargicin or cyclopiazonic acid rapidly activated ICRAC in low buffer
124 ompounds, including caffeine, ryanodine, and cyclopiazonic acid, reduce inhibitory junction potential
125 In addition, thapsigargin, ryanodine, and cyclopiazonic acid reduced action potential-evoked Ca2+
127 ER by exposure to the ER Ca2+ pump inhibitor cyclopiazonic acid resulted in a delayed activation of C
128 oxic challenge, thapsigargin, ryanodine, and cyclopiazonic acid resulted in a significant increase in
129 of the response to several concentrations of cyclopiazonic acid revealed that Ca2+ influx that regula
130 c levels) is achieved by a thapsigargin (and cyclopiazonic acid)-sensitive Ca2+-pump in cooperation w
131 ly Ca(2+)-free solution containing 10 microM cyclopiazonic acid, simultaneous 10(-6) M ET-1 and extra
132 taroxime accelerated and its inhibition with cyclopiazonic acid slowed TAUlocal significantly more in
134 litation was abolished by both ryanodine and cyclopiazonic acid suggesting a role for release from in
136 l smooth muscle hyperpolarizations evoked by cyclopiazonic acid were depressed by the gap junction in
137 tors of the SR calcium ATPase (thapsigargin, cyclopiazonic acid) were without effect on arterial wall
138 or Na+ but is abolished by thapsigargin and cyclopiazonic acid, which are specific inhibitors of the
139 (an inhibitor of IP8 formation) or 10 microM cyclopiazonic acid, which depletes intracellular Ca2+ st
141 confirmed by inhibiting SR Ca2+ ATPase with cyclopiazonic acid, which slowed Ca2+ removal more in co