PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21663732-6 2011 Additionally, thapsigargin, endoplasmic reticulum Ca(2+) pump inhibitor, completely inhibited BK-induced increase of intracellular Ca(2+). Thapsigargin 14-26 kininogen 1 Homo sapiens 94-96 28499726-4 2017 Bradykinin-induced [Ca2+]i increase was inhibited by the exposure to thapsigargin, which depletes Ca2+ stores on endoplasmic reticulum, but not by the exclusion of extracellular Ca2+. Thapsigargin 69-81 kininogen 1 Homo sapiens 0-10 17395626-8 2007 Likewise, wortmannin restored bradykinin-induced M-current inhibition when Ca(2)+ release was prevented with thapsigargin. Thapsigargin 109-121 kininogen 1 Homo sapiens 30-40 12594217-2 2003 After depletion of Ca(2+) stores by either TG, BK, or CCh, the addition of Ca(2+) gave a much larger rise in Ca(2+) levels in CCh-treated and TG-treated cells than in cells treated with BK. Thapsigargin 142-144 kininogen 1 Homo sapiens 186-188 12384249-10 2002 The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME. Thapsigargin 68-80 kininogen 1 Homo sapiens 22-32 12867160-4 2003 Thapsigargin, an inhibitor of Ca(2+)-ATPase in inositol 1,4,5-trisphosphate-sensitive Ca(2+) stores, mimicked the effect of bradykinin and histamine. Thapsigargin 0-12 kininogen 1 Homo sapiens 124-134 12867160-5 2003 In the fibroblasts pretreated with tyrosine kinase inhibitors, the bradykinin-, histamine- and thapsigargin-induced Ca(2+) entry was clearly enhanced, but not the transient [Ca(2+)](i) increase. Thapsigargin 95-107 kininogen 1 Homo sapiens 67-77 12384249-12 2002 Thus bradykinin reduced TEER through B(2) receptor-linked release of Ca(2+) from thapsigargin-sensitive stores, leading to activation of PLA(2) and metabolism of arachidonic acid by 5-lipoxygenase. Thapsigargin 81-93 kininogen 1 Homo sapiens 5-15 12088864-4 2002 Depletion of intracellular Ca(2+) store with thapsigargin abolished both the BK-induced Ca(2+) peak and sustained plateau. Thapsigargin 45-57 kininogen 1 Homo sapiens 77-79 8723904-6 1996 Experiments with thapsigargin (TG), BK, and PDGF indicated that BK and PDGF share intracellular Ca2+ pools that are sensitive to TG. Thapsigargin 17-29 kininogen 1 Homo sapiens 64-66 11352510-5 2001 In the primed fibroblasts, ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on the cyclooxygenase-2 mRNA expression. Thapsigargin 41-53 kininogen 1 Homo sapiens 90-100 11287092-8 2001 The calcium release induced by BK on the other hand was largely PTX-insensitive, PLC-dependent, and from both thapsigargin- and ryanodine-sensitive stores. Thapsigargin 110-122 kininogen 1 Homo sapiens 31-33 11805429-9 2001 CONCLUSIONS: Together, this study shows that bradykinin induced [Ca(2+)](i) increases in a concentration-dependent manner, by stimulating B2 bradykinin receptors leading to mobilization of Ca(2+) from the thapsigargin-sensitive stores in a manner dependent on inositol-1,4,5-trisphosphate, and also by inducing extracellular Ca(2+) influx. Thapsigargin 205-217 kininogen 1 Homo sapiens 45-55 11805429-9 2001 CONCLUSIONS: Together, this study shows that bradykinin induced [Ca(2+)](i) increases in a concentration-dependent manner, by stimulating B2 bradykinin receptors leading to mobilization of Ca(2+) from the thapsigargin-sensitive stores in a manner dependent on inositol-1,4,5-trisphosphate, and also by inducing extracellular Ca(2+) influx. Thapsigargin 205-217 kininogen 1 Homo sapiens 141-151 8672553-9 1996 Either Tg or FCCP reduced the calcium stores that could be released by BK or A23187. Thapsigargin 7-9 kininogen 1 Homo sapiens 71-73 11129088-7 2000 The results showed that 10 microM CLT: (i) inhibits the BK-induced proliferation of HSMC by 45-50%: (ii) prevents the rise of [Ca2+]i induced by BK (120.8 +/- 12.4 nM vs. 235.8 +/- 34.1 nM), an cffect similar to that of "classic" L-type calcium channels blockers: (iii) reduces the release of Ca2+ entry induced by thapsigargin suggesting a possible inhibition of the capacitative Ca2+ entry. Thapsigargin 315-327 kininogen 1 Homo sapiens 145-147 10812056-7 2000 In the fibroblasts pretreated with interleukin-1beta, Ca(2+)-mobilizing reagents such as ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on prostaglandin E(2) release. Thapsigargin 103-115 kininogen 1 Homo sapiens 152-162 7595498-4 1995 Thapsigargin (1 microM) pretreatment abolished the subsequent BK- and CCh-induced [Ca2+]i rise, though it did not affect agonist-induced IP3 generation. Thapsigargin 0-12 kininogen 1 Homo sapiens 62-64 7558231-6 1995 Similarly, the calcium-ATPase inhibitor thapsigargin, given at a dose (1 mumol/L) that abolished bradykinin-induced increases in intracellular calcium concentration in cultured porcine coronary artery endothelial cells, eliminated both bradykinin-induced. Thapsigargin 40-52 kininogen 1 Homo sapiens 97-107 7558231-6 1995 Similarly, the calcium-ATPase inhibitor thapsigargin, given at a dose (1 mumol/L) that abolished bradykinin-induced increases in intracellular calcium concentration in cultured porcine coronary artery endothelial cells, eliminated both bradykinin-induced. Thapsigargin 40-52 kininogen 1 Homo sapiens 236-246 7558231-8 1995 Although thapsigargin abolished bradykinin-induced prostaglandin I2 production, the basal production of prostaglandin I2 was enhanced and contraction of endothelium-intact rings was attenuated. Thapsigargin 9-21 kininogen 1 Homo sapiens 32-42 7582546-11 1995 The transient phase induced by BK, histamine and carbachol was inhibited in a time-dependent way by preincubation of the cells with thapsigargin. Thapsigargin 132-144 kininogen 1 Homo sapiens 31-33 7550072-4 1995 After depletion of the intracellular Ca2+ pool by thapsigargin, the increase in [Ca2+]i induced by bradykinin was obviously reduced. Thapsigargin 50-62 kininogen 1 Homo sapiens 99-109 7861149-7 1995 At low [Ca2+]e, thapsigargin abolished elevation of [Ca2+]i in response to methacholine and bradykinin and completely inhibited their stimulation of [3H]NA release. Thapsigargin 16-28 kininogen 1 Homo sapiens 92-102 1531101-4 1992 However, bradykinin-induced mobilization of the IP3-sensitive intracellular Ca2+ pool only partially reduced the subsequent response of cells to TG and BHQ. Thapsigargin 145-147 kininogen 1 Homo sapiens 9-19 8279522-2 1993 In adrenal medulla endothelial cells, we found that ATP and bradykinin could activate Ca2+ influx, although Ca2+ influx did not appear to be due to depletion of intracellular Ca2+ pools per se, since depletion of intracellular Ca2+ pools with thapsigargin reduced rather than enhanced both unidirectional and steady-state 45Ca2+ uptake. Thapsigargin 243-255 kininogen 1 Homo sapiens 60-70 8279522-5 1993 Bradykinin-induced cGMP and PGI2 formation and ATP-induced PGI2 formation each required Ca2+ release from intracellular Ca2+ pools, since depletion of these pools with thapsigargin inhibited their formation. Thapsigargin 168-180 kininogen 1 Homo sapiens 0-10 8396347-9 1993 The preconditioning and thapsigargin studies are consistent with a modulation of calcium extrusion processes by BK in CVEC. Thapsigargin 24-36 kininogen 1 Homo sapiens 112-114 8489507-10 1993 As with BK, the peak [Ca2+]i reached after thapsigargin treatment was higher at 22 degrees C. This effect of lower temperature on [Ca2+]i was most probably due to decreased Ca2+ efflux after a decrease in activity of the Ca(2+)-ATPase on the plasma membrane. Thapsigargin 43-55 kininogen 1 Homo sapiens 8-10 8130263-1 1994 The release of arachidonic acid in A549 cells was stimulated in a time- and dose-dependent manner by the Ca2+ ionophore ionomycin (t1/2 = 4 min), thapsigargin (t1/2 = 8 min), bradykinin (t1/2 = 12 min, EC50 = 3 nM), and interleukin 1 alpha (t1/2 = 28 min, EC50 = 0.3 ng/ml). Thapsigargin 146-158 kininogen 1 Homo sapiens 175-185 1875911-8 1991 Furthermore, the Ca2+ signals elicited by both bradykinin and epidermal growth factor were blocked in cells microinjected with the inositol 1,4,5-trisphosphate receptor antagonist heparin, whereas the intracellular Ca(2+)-ATPase inhibitor thapsigargin still mobilized Ca2+. Thapsigargin 239-251 kininogen 1 Homo sapiens 47-57