PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31415758-5 2019 This effect was abolished by treating cells with mechano-gated channel inhibitors, such as gadolinium, transient receptor potential (TRP) family inhibitor, ruthenium red, and with pharmacological and small interfering RNA-mediated TRPV1 inhibition. Ruthenium Red 156-169 transient receptor potential cation channel subfamily V member 1 Homo sapiens 231-236 32149229-4 2020 In contrast, addition of capsaicin to TRPV1-expressing HEK293 cells containing an optimum amount of a TRPV1 antagonist (ruthenium red), resulted in no detectable magnetic or fluorescent signals. Ruthenium Red 120-133 transient receptor potential cation channel subfamily V member 1 Homo sapiens 102-107 28782267-5 2017 LFEx and 4,5-di-O-CQA (EC50 = 69.34 +- 1.12 muM) activated TRPV1, and these activations were significantly inhibited by ruthenium red, a general blocker of TRP channels, and capsazepine, a specific antagonist of TRPV1. Ruthenium Red 121-134 transient receptor potential cation channel subfamily V member 1 Homo sapiens 60-65 30226565-5 2018 Suppression of TRPV1 activity by treatment with the TRPV1 antagonists capsazepine and ruthenium red significantly reduced UV-induced GSDMC expression, whereas direct activation of TRPV1 by capsaicin, a TRPV1 agonist, increased GSDMC expression. Ruthenium Red 86-99 transient receptor potential cation channel subfamily V member 1 Homo sapiens 15-20 30226565-5 2018 Suppression of TRPV1 activity by treatment with the TRPV1 antagonists capsazepine and ruthenium red significantly reduced UV-induced GSDMC expression, whereas direct activation of TRPV1 by capsaicin, a TRPV1 agonist, increased GSDMC expression. Ruthenium Red 86-99 transient receptor potential cation channel subfamily V member 1 Homo sapiens 52-57 30226565-5 2018 Suppression of TRPV1 activity by treatment with the TRPV1 antagonists capsazepine and ruthenium red significantly reduced UV-induced GSDMC expression, whereas direct activation of TRPV1 by capsaicin, a TRPV1 agonist, increased GSDMC expression. Ruthenium Red 86-99 transient receptor potential cation channel subfamily V member 1 Homo sapiens 52-57 30226565-5 2018 Suppression of TRPV1 activity by treatment with the TRPV1 antagonists capsazepine and ruthenium red significantly reduced UV-induced GSDMC expression, whereas direct activation of TRPV1 by capsaicin, a TRPV1 agonist, increased GSDMC expression. Ruthenium Red 86-99 transient receptor potential cation channel subfamily V member 1 Homo sapiens 52-57 28722259-6 2017 In TRPV1-transfected HEK293 cells, Orn and Lys (10 mM) evoked Ca2+ influx, which was blocked by ruthenium red, a TRP channel antagonist. Ruthenium Red 96-109 transient receptor potential cation channel subfamily V member 1 Homo sapiens 3-8 28782267-5 2017 LFEx and 4,5-di-O-CQA (EC50 = 69.34 +- 1.12 muM) activated TRPV1, and these activations were significantly inhibited by ruthenium red, a general blocker of TRP channels, and capsazepine, a specific antagonist of TRPV1. Ruthenium Red 121-134 transient receptor potential cation channel subfamily V member 1 Homo sapiens 213-218 27722942-8 2016 Control experiments with non TRPV1 channel expressing HEK cells as well as experiments with the TRPV1 channel blocker ruthenium red validated the specificity of the observed impedance decrease. Ruthenium Red 118-131 transient receptor potential cation channel subfamily V member 1 Homo sapiens 96-101 23307583-5 2013 These effects were completely abolished when neurons were preincubated with calcium-free bath solution or ruthenium-red (5 microM) and capsazepine (10 microM), suggesting the possibility of TRPV1 channel-activation by (-)-carvone. Ruthenium Red 106-119 transient receptor potential cation channel subfamily V member 1 Homo sapiens 190-195 24586504-5 2014 NGCC-induced Ca(2+) influx was significantly attenuated by ruthenium red (RR; 30 microM), a non-specific blocker of TRP channels and capsazepine (CZP; 5 microM), a specific antagonist of TRPV1, implying that NGCC directly activates hTRPV1. Ruthenium Red 59-72 transient receptor potential cation channel subfamily V member 1 Homo sapiens 187-192 24586504-5 2014 NGCC-induced Ca(2+) influx was significantly attenuated by ruthenium red (RR; 30 microM), a non-specific blocker of TRP channels and capsazepine (CZP; 5 microM), a specific antagonist of TRPV1, implying that NGCC directly activates hTRPV1. Ruthenium Red 59-72 transient receptor potential cation channel subfamily V member 1 Homo sapiens 232-238 24586504-5 2014 NGCC-induced Ca(2+) influx was significantly attenuated by ruthenium red (RR; 30 microM), a non-specific blocker of TRP channels and capsazepine (CZP; 5 microM), a specific antagonist of TRPV1, implying that NGCC directly activates hTRPV1. Ruthenium Red 74-76 transient receptor potential cation channel subfamily V member 1 Homo sapiens 187-192 24586504-5 2014 NGCC-induced Ca(2+) influx was significantly attenuated by ruthenium red (RR; 30 microM), a non-specific blocker of TRP channels and capsazepine (CZP; 5 microM), a specific antagonist of TRPV1, implying that NGCC directly activates hTRPV1. Ruthenium Red 74-76 transient receptor potential cation channel subfamily V member 1 Homo sapiens 232-238 23707350-3 2013 Further experiments showed that the SNP-induced [Ca(2+)]c increase was specifically blocked by potent antagonists of the transient receptor potential vanilloid subtype 1 (TRPV1) channel: capsazepine, ruthenium red, and La(3+) in Ca(2+)-containing buffer. Ruthenium Red 200-213 transient receptor potential cation channel subfamily V member 1 Homo sapiens 121-169 21315802-4 2011 We found that ruthenium red (RR; a nonselective TRP inhibitor) and AP18 (a TRPA1 antagonist) significantly increased scratching bouts caused by ET-1, while capsazepine (a TRPV1 antagonist) and morphine showed no effects in the ET-1-induced scratching response. Ruthenium Red 14-27 transient receptor potential cation channel subfamily V member 1 Homo sapiens 171-176 22327830-9 2012 Whereas the TRPV1 agonist capsaicin (CAP) (5-20 muM) -induced Ca(2+) transients were blocked by capsazepine (CPZ) (10 muM), the TRPV4 activator 4alpha-PDD (10 muM) -induced Ca(2+) increases were reduced by ruthenium-red (RuR) (20 muM). Ruthenium Red 206-219 transient receptor potential cation channel subfamily V member 1 Homo sapiens 12-17 21506114-6 2011 In fura2-loaded HCEC, a TRPV1-3 selective agonist, 100 microM 2-aminoethoxydiphenyl borate (2-APB), induced intracellular Ca(2+) transients and an increase in non-selective cation outward currents that were suppressed by ruthenium-red (RuR) (10-20 microM), a non-selective TRPV channel blocker. Ruthenium Red 221-234 transient receptor potential cation channel subfamily V member 1 Homo sapiens 24-29 21506114-6 2011 In fura2-loaded HCEC, a TRPV1-3 selective agonist, 100 microM 2-aminoethoxydiphenyl borate (2-APB), induced intracellular Ca(2+) transients and an increase in non-selective cation outward currents that were suppressed by ruthenium-red (RuR) (10-20 microM), a non-selective TRPV channel blocker. Ruthenium Red 236-239 transient receptor potential cation channel subfamily V member 1 Homo sapiens 24-29 24009849-7 2012 In addition, the intracellular Ca(2+) influx attained with KPEx to hTRPV1 was mostly blocked by ruthenium red, and capsazepine, a specific antagonist of TRPV1. Ruthenium Red 96-109 transient receptor potential cation channel subfamily V member 1 Homo sapiens 67-73 24009849-7 2012 In addition, the intracellular Ca(2+) influx attained with KPEx to hTRPV1 was mostly blocked by ruthenium red, and capsazepine, a specific antagonist of TRPV1. Ruthenium Red 96-109 transient receptor potential cation channel subfamily V member 1 Homo sapiens 68-73 19206161-5 2009 UV irradiation induced slow and persistent calcium influx and increased membrane current, which was inhibited by TRPV1 inhibitors (capsazepine and ruthenium red). Ruthenium Red 147-160 transient receptor potential cation channel subfamily V member 1 Homo sapiens 113-118 19683814-3 2009 In PMA-stimulated microglia, ROS production was substantially reduced upon inhibition of the non-selective cation channel TRPV1 with La(3+), ruthenium red, capsazepine and 5-iodo-resinferatoxin. Ruthenium Red 141-154 transient receptor potential cation channel subfamily V member 1 Homo sapiens 122-127 17508360-5 2007 Capsaicin (CAP) (1-10 microM) increased nonselective cation channel whole cell currents (2.5-fold +/- 0.5-fold between -60 and 130 mV), resulting in calcium transients that were fully blocked by the TRPV1 antagonists capsazepine (CPZ) and ruthenium red, or removal of extracellular calcium. Ruthenium Red 239-252 transient receptor potential cation channel subfamily V member 1 Homo sapiens 199-204 15685214-4 2005 Piperine produced a clear agonist activity at the human TRPV1 receptor yielding rapidly activating whole-cell currents that were antagonised by the competitive TRPV1 antagonist capsazepine and the non-competitive TRPV1 blocker ruthenium red. Ruthenium Red 227-240 transient receptor potential cation channel subfamily V member 1 Homo sapiens 56-61 17332266-5 2007 EGTA and ruthenium red inhibited cell surface TRPV1 activity, but they did not prevent ER stress gene responses or cytotoxicity. Ruthenium Red 9-22 transient receptor potential cation channel subfamily V member 1 Homo sapiens 46-51 17508023-5 2007 Heat-shock-induced MMP-1 expression was decreased by treatment of the TRPV1 inhibitors (capsazepine and ruthenium red) or knockdown of TRPV1 using RNA interference in HaCaT cells. Ruthenium Red 104-117 transient receptor potential cation channel subfamily V member 1 Homo sapiens 70-75 14514756-4 2003 Moreover, eugenol caused elevation of [Ca(2+)](i), and this was completely abolished by both capsazepine and ruthenium red in VR1-expressing HEK 293 cells and TG neurons. Ruthenium Red 109-122 transient receptor potential cation channel subfamily V member 1 Homo sapiens 126-129 11752091-7 2002 Pretreatment with VR1 receptor antagonists capsazepine or ruthenium red block both the calcium and sodium responses to agonists, and block agonist-induced cell death in a concentration-dependent manner. Ruthenium Red 58-71 transient receptor potential cation channel subfamily V member 1 Homo sapiens 18-21 12151520-5 2002 In both cases these responses are observed at temperatures lower than those required to activate TRPV1 and can be inhibited reversibly by ruthenium red. Ruthenium Red 138-151 transient receptor potential cation channel subfamily V member 1 Homo sapiens 97-102 11698030-11 2001 This increase is blocked by ruthenium red, suggesting that this effect is mediated through the vanilloid VR1 receptor. Ruthenium Red 28-41 transient receptor potential cation channel subfamily V member 1 Homo sapiens 105-108 11226139-8 2001 Capsazepine and ruthenium red were both more potent at blocking the capsaicin response of human VR1 than rat VR1. Ruthenium Red 16-29 transient receptor potential cation channel subfamily V member 1 Homo sapiens 96-99