PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24634418-8 2016 Pretreating the MSCs with the mitogen-activated protein kinase (MAPK)/ERK kinase 1/2 (MEK1/2) inhibitor PD98059, or the PKA inhibitor H-89, significantly inhibited the induction of osteogenic markers, showing that EMF induction of osteogenesis was dependent on the ERK and PKA signalling pathways. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 134-138 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 120-123 30541912-8 2019 The 8-OH-DPAT-induced changes at the synaptic level were enhanced by PKA inhibition by H-89 and blocked by PKA activation with bucladesine. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 87-91 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 69-72 29107062-8 2017 microinjection of protein kinase A (PKA) inhibitor H-89 and Ca(2+)/calmodulin-dependent protein kinase II (CamKII) inhibitor KN-62. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 51-55 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 18-34 29107062-8 2017 microinjection of protein kinase A (PKA) inhibitor H-89 and Ca(2+)/calmodulin-dependent protein kinase II (CamKII) inhibitor KN-62. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 51-55 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 36-39 29035879-11 2017 The PKA inhibitor H-89 and anti-RAGE antibody inhibited the AGE-BSA-induced impairment of Ca2+ signaling and cAMP/PKA activation. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-7 29035879-11 2017 The PKA inhibitor H-89 and anti-RAGE antibody inhibited the AGE-BSA-induced impairment of Ca2+ signaling and cAMP/PKA activation. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 114-117 28523193-3 2017 The objective was to identify the mechanisms underlying the antidepressant response of acupuncture through PKA signaling pathway in depression rats by employing the PKA signaling pathway inhibitor H89 in in vivo experiments. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 197-200 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 107-110 28523193-3 2017 The objective was to identify the mechanisms underlying the antidepressant response of acupuncture through PKA signaling pathway in depression rats by employing the PKA signaling pathway inhibitor H89 in in vivo experiments. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 197-200 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 165-168 30144443-8 2018 The addition of the PKA inhibitor H-89 to the FSHR cultures suppressed the gonadotropin and forskolin induction of progesterone secretion. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 34-38 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 20-23 29276916-8 2017 Proteinkinase A (PKA) inhibitors KT5720, H-89 and Rp-adenosine-cAMP suppressed ISO-induced hyperpolarization in PV. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 41-45 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-15 29276916-8 2017 Proteinkinase A (PKA) inhibitors KT5720, H-89 and Rp-adenosine-cAMP suppressed ISO-induced hyperpolarization in PV. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 41-45 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 17-20 28899916-8 2017 Consistently, the effect of GD1a in restoring myelin membrane formation in the presence of fibronectin aggregates was abolished by the PKA inhibitor H89, whereas the effect of GD1a was mimicked by the PKA activator dibutyryl-cAMP. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 149-152 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 135-138 28559304-6 2017 The PKA inhibitor H89 suppressed HDAC8-Ser39 phosphorylation, H3 acetylation and Stx1a induction by forskolin in FRSK cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-21 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-7 24634418-8 2016 Pretreating the MSCs with the mitogen-activated protein kinase (MAPK)/ERK kinase 1/2 (MEK1/2) inhibitor PD98059, or the PKA inhibitor H-89, significantly inhibited the induction of osteogenic markers, showing that EMF induction of osteogenesis was dependent on the ERK and PKA signalling pathways. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 134-138 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 273-276 29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 13-17 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 35-51 27400965-7 2016 RESULTS: Acute exposure to 1 muM PGE2 augments the capsaicin-evoked release of iCGRP, and this effect is blocked by the PKA inhibitor H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 134-138 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 120-123 29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 13-17 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 53-56 29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 13-17 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 168-171 26968794-7 2016 Moreover, ERK activation seems to be protein kinase A (PKA)-dependent because inhibition of PKA with H-89 was sufficient to block the GLP-1-derived protective effect on beta cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 101-105 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 37-53 26968794-7 2016 Moreover, ERK activation seems to be protein kinase A (PKA)-dependent because inhibition of PKA with H-89 was sufficient to block the GLP-1-derived protective effect on beta cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 101-105 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 55-58 26968794-7 2016 Moreover, ERK activation seems to be protein kinase A (PKA)-dependent because inhibition of PKA with H-89 was sufficient to block the GLP-1-derived protective effect on beta cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 101-105 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 92-95 26659380-3 2016 The effects on these barrier functions were significantly reduced in the presence of the GLP-1 receptor antagonist exendin-3 (9-39) and the protein kinase A (PKA) inhibitor H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 173-177 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 140-156 26659380-3 2016 The effects on these barrier functions were significantly reduced in the presence of the GLP-1 receptor antagonist exendin-3 (9-39) and the protein kinase A (PKA) inhibitor H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 173-177 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 158-161 27829866-7 2016 These changes were partially blocked by a selective protein kinase A (PKA) inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H89), suggesting that the PKA/CREB pathway is potentially involved in the effects of EA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 148-151 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 52-68 27829866-7 2016 These changes were partially blocked by a selective protein kinase A (PKA) inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H89), suggesting that the PKA/CREB pathway is potentially involved in the effects of EA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 148-151 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 70-73 27829866-7 2016 These changes were partially blocked by a selective protein kinase A (PKA) inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H89), suggesting that the PKA/CREB pathway is potentially involved in the effects of EA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 148-151 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 174-177 24877623-8 2014 Blocking protein kinase A activation with H-89 abrogated the estradiol-induced neuroprogesterone synthesis. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 42-46 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 9-25 26399925-8 2015 Ex vivo studies showed that sitagliptin increased the phosphorylated cAMP response element-binding protein (CREB), which can be reversed by H-89 (a PKA inhibitor), not brefeldin A (an Epac inhibitor).Heme oxygenase-1(HO-1) expression was increased by a PKA agonist but not by an Epac agonist.HO-1expression was attenuated in KG-501 (a CREB inhibitor)-treated infarcted rats in the presence of a PKA agonist. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 140-144 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 148-151 26399925-8 2015 Ex vivo studies showed that sitagliptin increased the phosphorylated cAMP response element-binding protein (CREB), which can be reversed by H-89 (a PKA inhibitor), not brefeldin A (an Epac inhibitor).Heme oxygenase-1(HO-1) expression was increased by a PKA agonist but not by an Epac agonist.HO-1expression was attenuated in KG-501 (a CREB inhibitor)-treated infarcted rats in the presence of a PKA agonist. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 140-144 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 253-256 26399925-8 2015 Ex vivo studies showed that sitagliptin increased the phosphorylated cAMP response element-binding protein (CREB), which can be reversed by H-89 (a PKA inhibitor), not brefeldin A (an Epac inhibitor).Heme oxygenase-1(HO-1) expression was increased by a PKA agonist but not by an Epac agonist.HO-1expression was attenuated in KG-501 (a CREB inhibitor)-treated infarcted rats in the presence of a PKA agonist. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 140-144 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 253-256 25349921-5 2014 H-89, a protein kinase A (PKA) inhibitor, attenuated the protective effect of TNFalpha when the cardiomyoctyes were subjected to hypoxia, as determined by lactate dehydrogenase (LDH) and creatine kinase (CK) released and from the cardiomyocytes. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 8-24 25349921-5 2014 H-89, a protein kinase A (PKA) inhibitor, attenuated the protective effect of TNFalpha when the cardiomyoctyes were subjected to hypoxia, as determined by lactate dehydrogenase (LDH) and creatine kinase (CK) released and from the cardiomyocytes. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 26-29 25306914-6 2015 Hyperphosphorylation was abrogated in the presence of protein kinase A and protein kinase C inhibitors H89 (20 muM) and staurosporine (10 nM), respectively, as well as by specific antagonists to N-methyl-D-aspartate (50 microM DL-AP5) and metabotropic glutamate receptor 1 (100 microM MPEP). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 103-106 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 54-70 25449602-9 2015 The rapid activation of eNOS by CMT was blocked by a highly selective PKA (protein kinase A) inhibitor H89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 103-106 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 70-73 25449602-9 2015 The rapid activation of eNOS by CMT was blocked by a highly selective PKA (protein kinase A) inhibitor H89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 103-106 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 75-91 24220689-7 2014 Dopamine D1 receptors lead to activation of protein kinase A (PKA), and including the PKA inhibitor H-89 or KT 5720 in the recording pipette solution prevented the facilitation of EPSCs. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 100-104 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 44-60 24412535-6 2014 The PKA inhibitor H-89 also reduced basal ICa; however, the inhibitory effects of C3SD and H-89 on basal ICa amplitude were not summative. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-7 24406203-5 2014 Pretreatment with H89, a protein kinase A (PKA) inhibitor, blocked IL-1beta-induced mechanical allodynia but not thermal hyperalgesia. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-21 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 25-41 24406203-5 2014 Pretreatment with H89, a protein kinase A (PKA) inhibitor, blocked IL-1beta-induced mechanical allodynia but not thermal hyperalgesia. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-21 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 43-46 24220689-7 2014 Dopamine D1 receptors lead to activation of protein kinase A (PKA), and including the PKA inhibitor H-89 or KT 5720 in the recording pipette solution prevented the facilitation of EPSCs. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 100-104 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 62-65 24220689-7 2014 Dopamine D1 receptors lead to activation of protein kinase A (PKA), and including the PKA inhibitor H-89 or KT 5720 in the recording pipette solution prevented the facilitation of EPSCs. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 100-104 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 86-89 23949609-4 2013 In this study, we investigated the effect of H-89, a selective inhibitor of PKA, on the neurite retraction along with evaluation of cell death and inflammatory markers in the differentiated PC12 cells, exposed to H2O2. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 45-49 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 76-79 23949609-5 2013 We found that dose-dependent inhibition of PKA by low and medium concentrations of H-89 (5, 7 and 10 muM) enhanced the parameters of neurite outgrowth and complexity in the cells co-treated with H2O2 as an oxidative stress. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 83-87 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 43-46 22933300-10 2012 The beta-adrenergic receptor antagonist propranolol or the PKA inhibitor H-89 completely blocked isoproterenol + IBMX-induced increase on surface NKCC2, while propranolol or H-89 alone had no effect. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 73-77 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 59-62 24015194-10 2013 In an ex vivo study, enhanced connexin43 levels afforded by N-acetylcysteine were partially blocked by either H-89 (a PKA inhibitor) or brefeldin A (an Epac-signaling inhibitor) and completely blocked when H-89 and brefeldin A were given in combination. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 110-114 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 118-121 23594614-6 2013 PKA blocker H-89 only reduced the plateau response (~41%), whereas the TASK-1-like K+ channel blocker/transient receptor potential vanilloid 1 channel agonist anandamide only inhibited the peak response (~48%), suggesting involvement of additional pathways. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 12-16 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-3 23000625-8 2012 This effect was changed by both the protein kinase A (PKA) inhibitor H89 (P<0.01, P<0.05, respectively, vs. Ex-4 group) and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 (P<0.01, P<0.01, respectively, vs. Ex-4 group) but not by the mitogen-activated protein kinase (MAPK) inhibitor U0126. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 69-72 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 54-57 22952280-5 2012 The inhibitory effect of UGN was completely abolished by either the protein kinase G (PKG) inhibitor KT5823 or by the protein kinase A (PKA) inhibitor H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 151-155 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 118-134 22952280-5 2012 The inhibitory effect of UGN was completely abolished by either the protein kinase G (PKG) inhibitor KT5823 or by the protein kinase A (PKA) inhibitor H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 151-155 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 136-139 23211299-6 2012 Conversely, selective protein kinase A inhibitors: H-89 (10 muM) and KT5720 (0.5 muM) increased the open probability of the GIRK-like channels. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 51-55 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-38 22515300-10 2012 Furthermore, intrathecal H-89 (a PKA inhibitor) significantly attenuated bone cancer pain behaviors in rats. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 25-29 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 33-36 20640531-4 2011 Pretreatment with H-89, a specific PKA antagonist, could completely reverse the effect of 6-Bnz-cAMP on cytokines expressions and kinases activities but had no effect on the performance of 8-pCPT-2"-O-Me-cAMP. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 35-38 22100641-9 2012 The PKA-blocker H-89 (10 mug/kg) was administered with and without helium (He-PC+H-89, H-89). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 16-20 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-7 21211029-5 2011 Subsequent work using both cell-attached and whole cell configurations revealed that the PKG and PKA inhibitors, KT5823 (3 muM) and H-89 (10 muM), also stimulated SOC activity; this augmentation was attenuated by the SOC blockers SKF-96365 (10 muM) and Ni2+ (0.1 mM). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 132-136 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 97-100 21963493-8 2011 The effects of these analogs were antagonized by the protein kinase A (PKA) inhibitor H-89 (10(-7) M). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 86-90 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 53-69 21963493-8 2011 The effects of these analogs were antagonized by the protein kinase A (PKA) inhibitor H-89 (10(-7) M). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 86-90 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 71-74 20118742-5 2010 Protein kinase A inhibitor H89 could not reverse above phenomenon, but played a synergistic effect on the contrary. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 27-30 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-16 20953210-7 2010 PKA inhibitor H-89 abolished swelling-induced transient increase of I(Ca,L), but did not affect the swelling-induced sustained decrease of I(Ca,L). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 14-18 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-3 20229011-12 2010 Only H-89, an inhibitor of protein kinase A (PKA), may reverse the decrease in disaccharidase activities and SI complex mRNA expression induced by berberine. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 5-9 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 27-43 20229011-12 2010 Only H-89, an inhibitor of protein kinase A (PKA), may reverse the decrease in disaccharidase activities and SI complex mRNA expression induced by berberine. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 5-9 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 45-48 20561511-5 2010 Forskolin (PKA activator) and H-89 (PKA inhibitor) also individually increased mIPSCs frequency, with an additional increase induced by co-incubation with bilirubin and H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 30-34 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 36-39 20463231-10 2010 Furthermore, the development of amphetamine CPP is significantly attenuated by intra-VTA infusion of the PKA inhibitor H89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 119-122 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 105-108 19398497-11 2009 Meanwhile, forskolin significantly inhibited IL-1beta-induced iNOS protein, which was reversed by H-89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 98-102 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 106-122 18670897-6 2009 The identification of the calcium signalling pathways were studied by applying U73122, an inhibitor of PL-C, and H-89, an inhibitor of protein kinase A (PKA), showing the involvement of PL-C/IP3 pathway but not the PKA/cAMP pathway. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 113-117 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 135-151 18670897-6 2009 The identification of the calcium signalling pathways were studied by applying U73122, an inhibitor of PL-C, and H-89, an inhibitor of protein kinase A (PKA), showing the involvement of PL-C/IP3 pathway but not the PKA/cAMP pathway. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 113-117 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 153-156 19398497-11 2009 Meanwhile, forskolin significantly inhibited IL-1beta-induced iNOS protein, which was reversed by H-89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 98-102 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 124-127 18207734-9 2008 Further experiments, in which insulin was replaced by H-89, revealed that the antilipolytic action of protein kinase A inhibitor on epinephrine-induced lipolysis was not affected by genistein. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 54-58 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 102-118 18694792-7 2008 Conversely, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89), an inhibitor of protein kinase A (PKA), that prevents the formation of pCREB induced by nontoxic NMDA concentrations, reverted the neuroprotection achieved by preincubation of low micromolar NMDA concentrations. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 12-72 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 96-112 18694792-7 2008 Conversely, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89), an inhibitor of protein kinase A (PKA), that prevents the formation of pCREB induced by nontoxic NMDA concentrations, reverted the neuroprotection achieved by preincubation of low micromolar NMDA concentrations. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 12-72 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 114-117 17392733-11 2008 H-89, a selective protein kinase A (PKA) inhibitor, decreased the frequencies of GABAergic mIPSCs and glutamatergic mEPSCs, and blocked their reduction by 5-HT. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 18-34 17392733-11 2008 H-89, a selective protein kinase A (PKA) inhibitor, decreased the frequencies of GABAergic mIPSCs and glutamatergic mEPSCs, and blocked their reduction by 5-HT. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 36-39 17478051-10 2007 A selective protein kinase A inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-soquinolinesulfonamide (H-89), inhibited the excitatory effect by isoproterenol. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 100-104 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 12-28 17680988-5 2007 Inhibition of PKA activity with H89 or ketoconazole abolished the effects of epinephrine on CREB, suggesting that activation of the cAMP/PKA pathway by AA epoxy-derivatives is responsible for CREB activation by alpha2-ARs. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 32-35 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 14-17 17350613-6 2007 Furthermore, both the adenylyl cyclase inhibitor SQ-22536 and the protein kinase A (PKA) inhibitor H-89 reversed the protection and the GABA release by clobenpropit. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 99-103 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 66-82 17350613-6 2007 Furthermore, both the adenylyl cyclase inhibitor SQ-22536 and the protein kinase A (PKA) inhibitor H-89 reversed the protection and the GABA release by clobenpropit. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 99-103 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 84-87 17303647-10 2007 The protein kinase A (PKA) inhibitor H-89 inhibited NPPB-induced outward current at 0 mV. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 17498241-4 2007 H89, a protein kinase A (PKA) inhibitor attenuated the PACAP response. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-3 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 7-23 17498241-4 2007 H89, a protein kinase A (PKA) inhibitor attenuated the PACAP response. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-3 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 25-28 17452290-8 2007 The protein kinase A (PKA) inhibitor H89 at a dose that completely blocked the PKA activator (8-br-cAMP)-induced CREB phosphorylation partially blocked the PMA-stimulated CREB phosphorylation. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 17452290-8 2007 The protein kinase A (PKA) inhibitor H89 at a dose that completely blocked the PKA activator (8-br-cAMP)-induced CREB phosphorylation partially blocked the PMA-stimulated CREB phosphorylation. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 17452290-8 2007 The protein kinase A (PKA) inhibitor H89 at a dose that completely blocked the PKA activator (8-br-cAMP)-induced CREB phosphorylation partially blocked the PMA-stimulated CREB phosphorylation. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 79-82 17303647-10 2007 The protein kinase A (PKA) inhibitor H-89 inhibited NPPB-induced outward current at 0 mV. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 17409628-9 2007 The effects of these analogs were antagonized by the protein kinase A (PKA) inhibitor H-89 (10(-7) M) and the protein kinase C (PKC) inhibitor sphingosine (10(-6) M), respectively. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 86-90 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 53-69 17318879-3 2007 The effect of SKF 38393 was mimicked by 1 mM 8-bromo-cyclic AMP (Br-cAMP) and inhibited by the protein kinase A (PKA) inhibitor H-89, mean inhibition 92% +/- 4% with 10 microM H-89 (n = 3). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 128-132 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 95-111 17318879-3 2007 The effect of SKF 38393 was mimicked by 1 mM 8-bromo-cyclic AMP (Br-cAMP) and inhibited by the protein kinase A (PKA) inhibitor H-89, mean inhibition 92% +/- 4% with 10 microM H-89 (n = 3). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 128-132 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 113-116 17409628-9 2007 The effects of these analogs were antagonized by the protein kinase A (PKA) inhibitor H-89 (10(-7) M) and the protein kinase C (PKC) inhibitor sphingosine (10(-6) M), respectively. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 86-90 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 71-74 17050780-6 2007 N6,2"-O-Dibutyryl-cAMP (dB-cAMP), when used at 0.5 mM, caused a down-regulation of Sig-1Rs that could be blocked by a protein kinase A (PKA) inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-89). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 229-233 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 118-134 17077345-7 2007 The in vitro addition of H-89, an inhibitor of protein kinase A (PKA), completely blocked the effect of PTX on the reduction of proteolysis in muscles from normal and diabetic rats. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 25-29 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 47-63 17077345-7 2007 The in vitro addition of H-89, an inhibitor of protein kinase A (PKA), completely blocked the effect of PTX on the reduction of proteolysis in muscles from normal and diabetic rats. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 25-29 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 65-68 17050780-6 2007 N6,2"-O-Dibutyryl-cAMP (dB-cAMP), when used at 0.5 mM, caused a down-regulation of Sig-1Rs that could be blocked by a protein kinase A (PKA) inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-89). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 229-233 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 136-139 17225460-11 2006 GF109203X, a protein kinase C (PKC) inhibitor and H89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 50-53 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 57-73 16501581-10 2006 5 ADM"s effect was abolished with H-89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 34-38 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 42-58 16859673-5 2006 H-89, a selective protein kinase A (PKA) inhibitor, blocked the vasorelaxant responses to genistein. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 18-34 16859673-5 2006 H-89, a selective protein kinase A (PKA) inhibitor, blocked the vasorelaxant responses to genistein. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 36-39 17174386-4 2006 H-89, a selective PKA II inhibitor, was administered into CA1 region of the hippocampus at 1, 2.5 and 5 microM/rat. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 18-21 16501581-10 2006 5 ADM"s effect was abolished with H-89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 34-38 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 60-63 16610234-6 2006 Forskolin, an adenylate cyclase activator, also enhanced Runx2 and osterix transcription, and the stimulatory effects of PTH and forskolin were blocked by the pre-treatment of the cells with H-89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 191-195 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 199-215 16527406-6 2006 The protein kinase A (PKA) inhibitor H89 reversed the chronic morphine-induced synaptic adaptation in GABA IPSCs. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 16527406-6 2006 The protein kinase A (PKA) inhibitor H89 reversed the chronic morphine-induced synaptic adaptation in GABA IPSCs. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 16487495-8 2006 The PKA inhibitor, H89, was a potent inhibitor of PACAP38-induced neurite outgrowth. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 19-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-7 16522741-5 2006 Instead, the cAMP-elevating agent forskolin induced cyclin D1 expression remarkably and this response was inhibited by pretreatment with H-89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 137-141 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 145-161 16522741-5 2006 Instead, the cAMP-elevating agent forskolin induced cyclin D1 expression remarkably and this response was inhibited by pretreatment with H-89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 137-141 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 163-166 16610234-6 2006 Forskolin, an adenylate cyclase activator, also enhanced Runx2 and osterix transcription, and the stimulatory effects of PTH and forskolin were blocked by the pre-treatment of the cells with H-89, a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 191-195 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 217-220 16143415-8 2005 Moreover, adenylate cyclase (AC) activator forskolin (n = 7) was observed to evoke GP neurons an excitatory response, whereas the histamine-induced excitation was effectively reduced by H-89 (n = 9), a selective and potent inhibitor of protein kinase A (PK(A)). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 186-190 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 236-252 16243961-11 2006 Inhibition of rho kinase, PKA, and PKG with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide.2HCl (H89) reduces carbachol maximum and carbachol potency. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 44-103 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 26-29 16243962-12 2006 Inhibition of rho kinase, PKA, and PKG with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide.2HCl (H89) increases darifenacin affinity. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 44-103 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 26-29 15813995-7 2005 MDL12330a, an adenylyl cyclase inhibitor, and H89, a protein kinase A (PKA) inhibitor, reversed the increase in glutamate synaptic transmission induced by chronic morphine. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 46-49 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 53-69 15772523-0 2005 H-89, a non-specific inhibitor of protein kinase A, promotes post-ischemic cardiac contractile recovery and reduces infarct size. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 34-50 15772523-4 2005 In another series, H-89 administered prior to preconditioning by 10 minutes of transient global ischemia decreased PKA activity (measured at the end of the preconditioning protocol) and augmented postischemic mechanical recovery. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 19-23 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 115-118 15772523-9 2005 PKA-inhibition by H-89 further decreased infarct size beyond preconditioning or forskolin. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-3 15750287-5 2005 The potentiation of SPLI release by bradykinin was reversed by HU210 or the protein kinase A (PKA) inhibitor H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 109-113 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 76-92 15750287-5 2005 The potentiation of SPLI release by bradykinin was reversed by HU210 or the protein kinase A (PKA) inhibitor H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 109-113 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 94-97 15813995-7 2005 MDL12330a, an adenylyl cyclase inhibitor, and H89, a protein kinase A (PKA) inhibitor, reversed the increase in glutamate synaptic transmission induced by chronic morphine. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 46-49 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 71-74 15522203-6 2004 Furthermore, 8-bromo-cAMP, an analogue of cAMP, mimicked the effect of AM, and H-89, an inhibitor for protein kinase A (PKA), significantly decreased the basal and AM-induced MMP-2 activity. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 79-83 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 102-118 15717845-6 2005 Inhibition of protein kinase A (PKA) by H-89 (50 micromol/l) slightly enhanced leptin release stimulated by glucose and leucine but not by alanine. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 40-44 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 14-30 15717845-6 2005 Inhibition of protein kinase A (PKA) by H-89 (50 micromol/l) slightly enhanced leptin release stimulated by glucose and leucine but not by alanine. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 40-44 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 32-35 15381705-9 2004 The protein kinase A (PKA) inhibitor H-89 and an inhibitory peptide for PKA abolished the caly A-evoked entry of both calcium and barium. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 15381705-9 2004 The protein kinase A (PKA) inhibitor H-89 and an inhibitory peptide for PKA abolished the caly A-evoked entry of both calcium and barium. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 15364618-7 2004 The effects of IPC on calpain, alpha-fodrin, and LDH release were blunted by the application of the PKA inhibitor H89 or alprenolol during IPC, while transient stimulation of PKA with CPT-cAMP or isoproterenol before ischemia attenuated calpain activation, alpha-fodrin degradation, and markedly reduced LDH release (P<0.001). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 114-117 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 100-103 15364618-7 2004 The effects of IPC on calpain, alpha-fodrin, and LDH release were blunted by the application of the PKA inhibitor H89 or alprenolol during IPC, while transient stimulation of PKA with CPT-cAMP or isoproterenol before ischemia attenuated calpain activation, alpha-fodrin degradation, and markedly reduced LDH release (P<0.001). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 114-117 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 175-178 15380675-4 2004 In this report, we show that prior administration of a PKA inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide ?2HCl (H-89; 0.36 mg/kg), significantly suppressed the elevation in Hsp70 mRNA (P < 0.05) and protein synthesis (P < 0.05) in male Sprague-Dawley rats following a single bout of exercise. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 70-129 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 55-58 15522203-6 2004 Furthermore, 8-bromo-cAMP, an analogue of cAMP, mimicked the effect of AM, and H-89, an inhibitor for protein kinase A (PKA), significantly decreased the basal and AM-induced MMP-2 activity. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 79-83 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 120-123 15242814-4 2004 Both the forskolin and the N(6)-monobutyryl cAMP activated PDE4 activities were blocked by the PKA-specific inhibitor, H89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 119-122 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 95-98 15133061-5 2004 The protein kinase A (PKA) inhibitor H89 (0.3 microM) and the competitive antagonist of cAMP binding to PKA, Rp-cAMPS, had weak or no effect on the action of pCPT-cAMP. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 15133061-5 2004 The protein kinase A (PKA) inhibitor H89 (0.3 microM) and the competitive antagonist of cAMP binding to PKA, Rp-cAMPS, had weak or no effect on the action of pCPT-cAMP. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 14615061-5 2003 Moreover, there was a three to four-fold increase in amylin promoter activity which was inhibited by the specific protein kinase A (PKA) inhibitor, H89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 148-151 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 114-130 15066141-10 2004 Addition of the specific protein kinase A inhibitor H89 in the patch pipette solution prevented the reduction of I(K) induced by both PACAP and dbcAMP. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 52-55 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 25-41 12869590-8 2003 All 2-iodomelatonin effects on Iout were sensitive to PTX treatment and the PKA inhibitor H-89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 90-94 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 76-79 14644761-8 2004 Protein kinase A inhibition by H89 also inhibited ADRF release, whereas the protein kinase G inhibitor KT-5823 had no effect. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 31-34 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-16 15127949-5 2003 Pretreatment of H89, an inhibitor of protein kinase A (PKA), failed to alter the AM- or PAMP-induced decreases in LVP and LVP +/- dp/dtmax, but further promoted the AM or PAMP increased CF. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 16-19 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 37-53 15127949-5 2003 Pretreatment of H89, an inhibitor of protein kinase A (PKA), failed to alter the AM- or PAMP-induced decreases in LVP and LVP +/- dp/dtmax, but further promoted the AM or PAMP increased CF. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 16-19 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 55-58 14615061-5 2003 Moreover, there was a three to four-fold increase in amylin promoter activity which was inhibited by the specific protein kinase A (PKA) inhibitor, H89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 148-151 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 132-135 12963496-1 2003 The present study was performed to clarify the effect of H89, an inhibitor of cAMP-activated protein kinase (protein kinase A; PKA), on Na(+) absorption in fetal rat alveolar type II epithelium. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 57-60 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 109-125 12963496-1 2003 The present study was performed to clarify the effect of H89, an inhibitor of cAMP-activated protein kinase (protein kinase A; PKA), on Na(+) absorption in fetal rat alveolar type II epithelium. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 57-60 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 127-130 14733413-10 2003 Protein kinase A (PKA) inhibitor H-89 significantly weakened the effects of AM. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 33-37 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-16 14733413-10 2003 Protein kinase A (PKA) inhibitor H-89 significantly weakened the effects of AM. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 33-37 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 18-21 12694408-4 2003 Consistent with this possibility the adenylate cyclase inhibitor MDL12,330A, and the PKA inhibitor H-89 prevented PNMT promoter stimulation by the combination of forskolin and PMA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 99-103 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 85-88 12865141-3 2003 The effects of KCl and forskolin were mediated via the protein kinase A (PKA) and the extracellular signal-regulated kinase (ERK) signaling pathways, since addition of the ERK kinase (MEK1) inhibitor PD98059 and the PKA inhibitor H89 inhibits neurite outgrowth. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 230-233 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 55-71 12372033-8 2002 The PKA-specific inhibitor, H-89, increased the AHP in neurons from all groups to a similar extent, and the difference in AHP amplitude between neurons from TR rats and neurons from controls was maintained. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 28-32 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-7 12456822-8 2002 In addition, we found that the reduction in the Kir current mediated by GHRP-2 was totally abolished by the pretreatments with H89 (1 microM) or Rp-cAMP (100 microM) or by intracellular dialysis of a specific protein kinase A (PKA) inhibitory peptide PKI (10 microM). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 127-130 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 209-225 12456822-8 2002 In addition, we found that the reduction in the Kir current mediated by GHRP-2 was totally abolished by the pretreatments with H89 (1 microM) or Rp-cAMP (100 microM) or by intracellular dialysis of a specific protein kinase A (PKA) inhibitory peptide PKI (10 microM). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 127-130 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 227-230 12530678-4 2002 Pretreatment of cells with the adenylyl cyclase (AC) inhibitor SQ 22536 or the protein kinase A (PKA) inhibitor H-89 markedly attenuated the effect of 5-HT on aldosterone secretion. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 112-116 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 79-95 12530678-4 2002 Pretreatment of cells with the adenylyl cyclase (AC) inhibitor SQ 22536 or the protein kinase A (PKA) inhibitor H-89 markedly attenuated the effect of 5-HT on aldosterone secretion. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 112-116 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 97-100 12538438-6 2003 Microinjection bilaterally into the NTS of the selective protein kinase A (PKA) inhibitor H-89 (100 pmol) or the selective PKC inhibitor calphostin C (100 pmol) significantly attenuated all of the above events induced in SHR by HS. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 90-94 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 57-73 12538438-6 2003 Microinjection bilaterally into the NTS of the selective protein kinase A (PKA) inhibitor H-89 (100 pmol) or the selective PKC inhibitor calphostin C (100 pmol) significantly attenuated all of the above events induced in SHR by HS. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 90-94 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 75-78 12355181-6 2002 Moreover, perfusion with 30 nM isoproterenol in the presence of the PKA inhibitor H-89 decreased phosphorylation at both PLB residues and diminished the inotropic and relaxant responses to the beta-agonist. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 82-86 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 68-71 12162494-8 2002 Finally, the greater than additive transactivation of CREB by PTH and EGF is significantly inhibited by the PKA inhibitor H-89 or by cotreatment with SB203580 and PD98059. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 122-126 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 108-111 11546650-6 2001 The kinase inhibitor H-89 reversed this inhibition, suggesting that regulation by cAMP involves a protein kinase A (PKA)-dependent process. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 21-25 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 98-114 12121497-6 2002 This CRF-induced reduction of CRF-R1 mRNA expression was inhibited completely by pretreatment with protein kinase A (PKA) inhibitor (1 microM H-89). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 142-146 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 99-115 12121497-6 2002 This CRF-induced reduction of CRF-R1 mRNA expression was inhibited completely by pretreatment with protein kinase A (PKA) inhibitor (1 microM H-89). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 142-146 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 117-120 12065610-6 2002 This was prevented by the D(1) receptor antagonist SCH 23390 and the protein kinase A inhibitor H89, and reproduced by forskolin. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 96-99 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 69-85 12028440-7 2002 Furthermore, the fact that the forskolin-induced potentiation of the [Ca2+]i response to Ang III was blocked by 10 micromol/L H-89, a specific protein kinase A (PKA) inhibitor, indicated that this effect occurred via activation of PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 126-130 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 143-159 12028440-7 2002 Furthermore, the fact that the forskolin-induced potentiation of the [Ca2+]i response to Ang III was blocked by 10 micromol/L H-89, a specific protein kinase A (PKA) inhibitor, indicated that this effect occurred via activation of PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 126-130 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 161-164 12028440-7 2002 Furthermore, the fact that the forskolin-induced potentiation of the [Ca2+]i response to Ang III was blocked by 10 micromol/L H-89, a specific protein kinase A (PKA) inhibitor, indicated that this effect occurred via activation of PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 126-130 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 231-234 11790809-8 2002 This inhibition was absent in the presence of the protein kinase A (PKA) inhibitor H-89, implying the involvement of PKA-mediated phosphorylation. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 83-87 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 50-66 11790809-8 2002 This inhibition was absent in the presence of the protein kinase A (PKA) inhibitor H-89, implying the involvement of PKA-mediated phosphorylation. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 83-87 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 68-71 11790809-8 2002 This inhibition was absent in the presence of the protein kinase A (PKA) inhibitor H-89, implying the involvement of PKA-mediated phosphorylation. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 83-87 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 117-120 12074893-9 2002 The protein kinase A inhibitor H-89 and the protein kinase C inhibitor chelerythrine could antagonize the effect of dopamine. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 31-35 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 11546650-6 2001 The kinase inhibitor H-89 reversed this inhibition, suggesting that regulation by cAMP involves a protein kinase A (PKA)-dependent process. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 21-25 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 116-119 11576743-7 2001 H89 (10 microM), another PKA inhibitor, also markedly decreased SA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-3 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 25-28 11559778-7 2001 The PKA inhibitor H-89 blocked both of these effects. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 18-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-7 11833426-8 2001 Pre-treatment of VSMCs with 100 nmol/L H-89, a protein kinase A (PKA) inhibitor, abolished the desensitization of CGRP-acting receptor, implying that this desensitization was mediated through PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 39-43 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 47-63 11833426-8 2001 Pre-treatment of VSMCs with 100 nmol/L H-89, a protein kinase A (PKA) inhibitor, abolished the desensitization of CGRP-acting receptor, implying that this desensitization was mediated through PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 39-43 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 65-68 11833426-8 2001 Pre-treatment of VSMCs with 100 nmol/L H-89, a protein kinase A (PKA) inhibitor, abolished the desensitization of CGRP-acting receptor, implying that this desensitization was mediated through PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 39-43 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 192-195 11763200-1 2001 This study investigated the effects of the protein kinase A (PKA) inhibitor, H-89, in mechanically-skinned muscle fibres and intact muscle fibres, in order to determine whether PKA phosphorylation is essential for normal excitation-contraction (E-C) coupling. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 77-81 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 61-64 11279288-3 2001 We infused the PKA inhibitor H-89 into the striatum of male rats, followed 30 min later by systemic administration of eticlopride. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 29-33 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 15-18 11160494-4 2001 Preincubation of slices with the PKA inhibitor H-89 abolished the effect of ACPT-1, as did preincubation with the adenylate cyclase inhibitor, SQ22536. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 47-51 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 33-36 11763200-2 2001 In skinned EDL fibres of the rat, force responses to depolarization (by ion substitution) were inhibited only slightly by 10 microM H-89, a concentration more than sufficient to fully inhibit PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 132-136 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 192-195 11013128-8 2000 Pretreatment with the beta -adrenergic antagonist propranolol (10(-5)m) or PKA inhibitor H-89 (10(-6)m) blocked the effects of isoproterenol, while either drug alone did not affect the gene transcription rate significantly. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 89-93 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 75-78 11006268-11 2000 The protein kinase A inhibitor H89 inhibited the stimulation of phosphorylation of p38-MAPKs by forskolin, whereas inhibitors of protein kinase C, p70(S6k), and phosphatidylinositol 3-kinase were ineffective. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 31-34 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 10934042-5 2000 These data and studies with the protein kinase A inhibitor, H-89, indicate that cAMP signaling plays a key role in enhanced assembly. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 60-64 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 32-48 10482800-6 1999 Protection by PACAPs (100 nM) against glutamate-induced neurotoxicity was antagonized by PACAP6-38 (1 microM), a PACAP antagonist, and H-89 (1 microM), a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 135-139 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 154-170 10564111-8 1999 Furthermore, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide, a cell-permeable inhibitor of protein kinase A (PKA), reduced the stimulation of oxygen uptake by PGE(2). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 13-72 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 104-120 10564111-8 1999 Furthermore, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide, a cell-permeable inhibitor of protein kinase A (PKA), reduced the stimulation of oxygen uptake by PGE(2). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 13-72 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 122-125 11019898-3 2000 The secretagogue effect of tyrphostin-23 on dispersed rat adrenocortical cells was abolished by either the adenylate cyclase inhibitor SQ-22536 (10(-4) M) or the protein kinase A (PKA) inhibitor H-89 (10(-5) M). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 195-199 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 180-183 10878598-9 2000 Pretreating cells with PKA inhibitor, H-89, prevented the effect of dibutyryl cAMP. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 38-42 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 23-26 10908723-3 2000 Whilst the protein kinase A inhibitor H89 ablated the ability of forskolin to cause cAMP response element binding protein (CREB) phosphorylation in Rat1 cells, it did not affect the ability of forskolin to activate either Rap1A and Rap1B. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 38-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 11-27 10750043-10 2000 Pre-incubation of cells with 100 nM H-89, a protein kinase A (PKA) inhibitor, abolished the desensitisation of CGRP by itself, implying that this desensitisation was mediated through PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 36-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 44-60 10750043-10 2000 Pre-incubation of cells with 100 nM H-89, a protein kinase A (PKA) inhibitor, abolished the desensitisation of CGRP by itself, implying that this desensitisation was mediated through PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 36-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 62-65 10750043-10 2000 Pre-incubation of cells with 100 nM H-89, a protein kinase A (PKA) inhibitor, abolished the desensitisation of CGRP by itself, implying that this desensitisation was mediated through PKA. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 36-40 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 183-186 10482800-6 1999 Protection by PACAPs (100 nM) against glutamate-induced neurotoxicity was antagonized by PACAP6-38 (1 microM), a PACAP antagonist, and H-89 (1 microM), a protein kinase A (PKA) inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 135-139 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 172-175 10374718-7 1999 Adrenomedullin-mediated decrease in proliferation and increase in apoptosis were inhibited by H89 [[N-[2-((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide, hydrochloride]], a potent protein kinase-A inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 94-97 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 189-205 10465510-9 1999 The corticosterone secretagogue action of 10(-7) M GIP was abolished by the protein kinase A (PKA) inhibitor H-89 (10(-5)M), and unaffected by CIP (10(-6)M). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 109-113 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 76-92 9829969-7 1998 Moreover, the specific PKA inhibitor H-89 blocked cAMP-induced but not NGF-induced up-regulation of CBP activity. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 23-26 10465510-9 1999 The corticosterone secretagogue action of 10(-7) M GIP was abolished by the protein kinase A (PKA) inhibitor H-89 (10(-5)M), and unaffected by CIP (10(-6)M). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 109-113 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 94-97 9556582-5 1998 Protein kinase A (PKA) inhibition by H-89 enhanced inositol phosphate formation stimulated by fMLP but not PAF. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-16 9789110-8 1998 On the other hand, the CMZ stimulation of IBa was prevented by both H-7, a nonspecific protein kinase inhibitor, and H-89, a specific inhibitor of protein kinase A (PK-A). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 117-121 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 147-163 9789110-8 1998 On the other hand, the CMZ stimulation of IBa was prevented by both H-7, a nonspecific protein kinase inhibitor, and H-89, a specific inhibitor of protein kinase A (PK-A). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 117-121 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 165-169 9794724-8 1998 Administration of a selective PKA inhibitor, H-89, significantly prevented induction of increases in expression of HSP70 mRNA and rates of synthesis of protein by a high pressure overload and exposure to agents that increase cAMP content. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 45-49 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 30-33 9556582-5 1998 Protein kinase A (PKA) inhibition by H-89 enhanced inositol phosphate formation stimulated by fMLP but not PAF. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 18-21 9501870-9 1998 The inductions of VEGF and bFGF mRNA expression by PGE2 were blocked by the specific PKA inhibitors H-89 (30 microM) or SQ 22536 (500 microM, 1000 microM). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 100-104 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 85-88 9458736-0 1998 PKA inhibitor, H-89, affects the intracellular transit of regulated secretory proteins in rat lacrimal glands. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 15-19 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-3 9458736-1 1998 We tested the effect of H-89, a protein kinase A (PKA) inhibitor, on the intracellular transit of the regulated secretory proteins in rat lacrimal glands. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 24-28 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 32-48 9458736-1 1998 We tested the effect of H-89, a protein kinase A (PKA) inhibitor, on the intracellular transit of the regulated secretory proteins in rat lacrimal glands. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 24-28 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 50-53 9458736-5 1998 The effect of H-89 seems to be due to PKA inhibition because other protein kinase inhibitors (calphostin C, chelerythrine, H-85) do not induce secretion. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 14-18 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 38-41 9275048-10 1997 The protein kinase A (PKA) inhibitors, H-89 (10 microM; 30 min) and dideoxyadenosine (5 nM; 10 min) significantly decreased the forskolin- and dbcAMP-mediated PLD activation without any effect on the phorbol ester-mediated PLD response. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 39-43 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 9570336-2 1998 Corticosterone responses to PP were abolished by the specific protein kinase A (PKA) antagonist H-89 (10[-5] M). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 96-100 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 62-78 9570336-2 1998 Corticosterone responses to PP were abolished by the specific protein kinase A (PKA) antagonist H-89 (10[-5] M). N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 96-100 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 80-83 9169858-10 1997 The membrane-permeable PKA inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89) did not suppress the induction of GFAP-mRNA and its translation into GFAP. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-97 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 23-26 9396033-6 1997 Inhibition of kainate-induced Ca2+ influx by ibudilast was decreased by H-89, a protein kinase A (PKA) inhibitor, but increased by okadaic acid, an inhibitor of phosphatase 1 and 2A. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 72-76 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 80-96 9396033-6 1997 Inhibition of kainate-induced Ca2+ influx by ibudilast was decreased by H-89, a protein kinase A (PKA) inhibitor, but increased by okadaic acid, an inhibitor of phosphatase 1 and 2A. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 72-76 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 98-101 9275048-10 1997 The protein kinase A (PKA) inhibitors, H-89 (10 microM; 30 min) and dideoxyadenosine (5 nM; 10 min) significantly decreased the forskolin- and dbcAMP-mediated PLD activation without any effect on the phorbol ester-mediated PLD response. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 39-43 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 9039126-5 1997 These actions are mimicked by forskolin 1 to 10 mumol/L, a direct activator of adenylate cyclase and 8-bromo-cAMP 0.1 to 1 mmol/L, and are blocked by a specific protein kinase A (PKA) inhibitor N-[2-(P-bromcoinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H89) but not blocked by its negative control. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 256-259 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 161-177 8896810-5 1996 H-89, a protein kinase A (PKA) inhibitor, increased the 10(-5) M Gly response but had little effect on the 10(-4) M Gly response. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 8-24 8896810-5 1996 H-89, a protein kinase A (PKA) inhibitor, increased the 10(-5) M Gly response but had little effect on the 10(-4) M Gly response. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 26-29 9039126-5 1997 These actions are mimicked by forskolin 1 to 10 mumol/L, a direct activator of adenylate cyclase and 8-bromo-cAMP 0.1 to 1 mmol/L, and are blocked by a specific protein kinase A (PKA) inhibitor N-[2-(P-bromcoinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H89) but not blocked by its negative control. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 256-259 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 179-182 7559463-9 1995 The involvement of PKA was verified when the highly specific PKA inhibitor, H-89, completely abolished the stimulatory effect of PTH(1-34) and forskolin on Na+/H+ exchange. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 76-80 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 19-22 8742021-4 1996 The cell death was attenuated by cycloheximide or by H-89, a specific protein kinase A (PKA) inhibitor, but not by H-7 or KN-62. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 53-57 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 70-86 8742021-4 1996 The cell death was attenuated by cycloheximide or by H-89, a specific protein kinase A (PKA) inhibitor, but not by H-7 or KN-62. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 53-57 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 88-91 7559463-9 1995 The involvement of PKA was verified when the highly specific PKA inhibitor, H-89, completely abolished the stimulatory effect of PTH(1-34) and forskolin on Na+/H+ exchange. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 76-80 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 61-64 34000337-6 2021 The protein kinase A (PKA) inhibitor H-89 reduced mechanical PGE2-induced hyperalgesia in OVX female rats, whereas no effect was observed in sham-operated animals. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 2156866-1 1990 A newly synthesized isoquinolinesulfonamide, H-89 (N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide), was shown to have a potent and selective inhibitory action against cyclic AMP-dependent protein kinase (protein kinase A), with an inhibition constant of 0.048 +/- 0.008 microM. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 45-49 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 218-234 34000337-6 2021 The protein kinase A (PKA) inhibitor H-89 reduced mechanical PGE2-induced hyperalgesia in OVX female rats, whereas no effect was observed in sham-operated animals. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-41 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 32931071-7 2020 Afterward, the application of Baclofen and H89 alleviated the IS-evoked hyperalgesia and extenuated vesicular glutamate transporter 2 (VGLUT2), glutamate, calcitonin gene-related peptide (CGRP), and c-Fos expression by regulating the GABABR2/PKA/SynCAM1 pathway in the PAG of CM rats, while the application of CGP35348 and 8-Bromo-cAMP exactly exerted the opposite effect. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 43-46 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 242-245 33300086-8 2021 Additionally, treatment with the protein kinase A antagonist H-89 inhibited the IMD-mediated cardioprotective effects, including SERCA activity restoration, anti-Ca2+ overload, endoplasmic reticulum stress inhibition and antiapoptosis effects. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 61-65 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 33-49 32973437-8 2020 Furthermore, the anti-nociceptive effect of EMD-386088 on neuropathic pain was prevented by the adenylate cyclase (AC) inhibitor SQ-22536, and protein kinase A (PKA) inhibitor H89, suggesting that AC/PKA signaling might underlie the antinociception of agonists. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 176-179 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 143-159 32926327-7 2021 H-89, a PKA inhibitor, suppressed PKA activation, ROS accumulation, and Nox4 activity in NRK-52E cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 8-11 32926327-7 2021 H-89, a PKA inhibitor, suppressed PKA activation, ROS accumulation, and Nox4 activity in NRK-52E cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 0-4 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 34-37 32973437-8 2020 Furthermore, the anti-nociceptive effect of EMD-386088 on neuropathic pain was prevented by the adenylate cyclase (AC) inhibitor SQ-22536, and protein kinase A (PKA) inhibitor H89, suggesting that AC/PKA signaling might underlie the antinociception of agonists. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 176-179 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 161-164 32376452-11 2020 The PKA activity-dependent ROF-induced effect in the IL was correlated with an increase in its brain-derived neurotrophic factor (BDNF) protein expression, while blockade of PKA with 10 microM H89 in the IL abolished the ROF-induced increase in BDNF expression and prevented the effect of ROF on extinction recall. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 193-196 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-7 32376452-11 2020 The PKA activity-dependent ROF-induced effect in the IL was correlated with an increase in its brain-derived neurotrophic factor (BDNF) protein expression, while blockade of PKA with 10 microM H89 in the IL abolished the ROF-induced increase in BDNF expression and prevented the effect of ROF on extinction recall. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 193-196 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 174-177 32319618-8 2020 Also, PKA activity in IEC-6 cells was increased by both exendin-4 and forskolin, whereas these effects were abolished by the pre-treatment of exendin-9, which is a GLP-1R inhibitor, SQ22536 and H89. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 194-197 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 6-9 31905925-4 2019 We also showed that (1) the AUR-induced GDNF production was inhibited by U0126, a specific inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) 1/2, and by H89, a specific inhibitor of protein kinase A (PKA); and (2) AUR induced the phosphorylation of cAMP response element-binding protein (CREB), a transcription factor located within the nucleus. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 193-196 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 222-238 31583569-6 2020 Subsequent to the addition of protein kinase A (PKA) blocker N-[2- (p-Bromocin-namylamino)ethyl]-5 -isoquinolinesulfonamide dihydrochloride (H-89) before CNP treatment, the inhibitory effect of CNP was reduced; subsequent to the addition of protein kinase G (PKG) blocker KT5823 before CNP treatment, the inhibitory effect of CNP was also reduced. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 141-145 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 48-51 31905925-4 2019 We also showed that (1) the AUR-induced GDNF production was inhibited by U0126, a specific inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) 1/2, and by H89, a specific inhibitor of protein kinase A (PKA); and (2) AUR induced the phosphorylation of cAMP response element-binding protein (CREB), a transcription factor located within the nucleus. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 193-196 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 240-243 31649530-8 2019 In addition, application of H89, a protein kinase A (PKA) inhibitor, suppressed the SBP-induced neurofilament expressions, as well as the phosphorylation of cAMP-responsive element binding protein (CREB) in cultures. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 28-31 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 35-51 31649530-8 2019 In addition, application of H89, a protein kinase A (PKA) inhibitor, suppressed the SBP-induced neurofilament expressions, as well as the phosphorylation of cAMP-responsive element binding protein (CREB) in cultures. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 28-31 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 53-56