PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22770428-7 2012 Inhibition of cAMP-dependent protein kinase [also known as protein kinase A (PKA)] by H89 mimicked the effect of ACPD, and the mGluR agonist had its actions reversed by artificially sustaining cAMP through the PDE (phosphodiesterase) inhibitor IBMX (isobutylmethylxanthine) or the cAMP mimetic dbcAMP (dibutyryl cAMP). Bucladesine 294-300 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 59-75 23613468-7 2013 Specifically, positive PKA modulators (db-cAMP, forskolin, isoproterenol) suppressed T-type currents and evoked a hyperpolarized shift in steady-state inactivation. Bucladesine 39-46 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 23-26 23576581-6 2013 In addition, the protein kinase A (PKA) inhibitor reversed the effects of db-cAMP on the expression of Nox4 and Gialpha proteins and hyperproliferation of VSMC from SHR to WKY levels, while stimulation of the exchange protein directly activated by cAMP did not have any effect on these parameters. Bucladesine 74-81 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 17-33 23576581-6 2013 In addition, the protein kinase A (PKA) inhibitor reversed the effects of db-cAMP on the expression of Nox4 and Gialpha proteins and hyperproliferation of VSMC from SHR to WKY levels, while stimulation of the exchange protein directly activated by cAMP did not have any effect on these parameters. Bucladesine 74-81 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 35-38 22770428-7 2012 Inhibition of cAMP-dependent protein kinase [also known as protein kinase A (PKA)] by H89 mimicked the effect of ACPD, and the mGluR agonist had its actions reversed by artificially sustaining cAMP through the PDE (phosphodiesterase) inhibitor IBMX (isobutylmethylxanthine) or the cAMP mimetic dbcAMP (dibutyryl cAMP). Bucladesine 294-300 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 77-80 22269608-6 2012 A potent inhibitor of protein kinase A (PKA), H89 (500 muM), potentiated the 8-Br-cAMP- and forskolin-induced increases in 2,3-DHBA and antagonized the inhibitory effect of 100 nmol of db-cAMP. Bucladesine 185-192 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-38 22269608-6 2012 A potent inhibitor of protein kinase A (PKA), H89 (500 muM), potentiated the 8-Br-cAMP- and forskolin-induced increases in 2,3-DHBA and antagonized the inhibitory effect of 100 nmol of db-cAMP. Bucladesine 185-192 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 40-43 17277021-5 2007 Activation of PKA (dibutyryl-cAMP, forskolin) or PKG (dibutyryl-cGMP, sodium nitroprusside, nitric oxide) similarly abolished the ability of UTP to suppress K(DR) and did so without effect on baseline current. Bucladesine 19-33 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 14-17 22916194-6 2012 The inhibition of both PTP and phosphorylation of PKA substrates by SACH could be restored by addition of cAMP analog dibutyryl-cAMP (dbcAMP) and phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). Bucladesine 118-132 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 50-53 22916194-6 2012 The inhibition of both PTP and phosphorylation of PKA substrates by SACH could be restored by addition of cAMP analog dibutyryl-cAMP (dbcAMP) and phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). Bucladesine 134-140 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 50-53 17960568-12 2008 DbcAMP-induced activation of the either the p38 or the ERK 1,2 MAPK pathways was abolished by either of the PKA inhibitors, H-89 or KT5720. Bucladesine 0-6 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 108-111 21460187-6 2011 dbcAMP-induced Rac1 activation was principally mediated by protein kinase A (PKA) and Sif- and Tiam1-like exchange factor (STEF)/Tiam2. Bucladesine 0-6 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 59-75 21460187-6 2011 dbcAMP-induced Rac1 activation was principally mediated by protein kinase A (PKA) and Sif- and Tiam1-like exchange factor (STEF)/Tiam2. Bucladesine 0-6 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 77-80 21460187-8 2011 PKA phosphorylates STEF at three residues (Thr-749, Ser-782, Ser-1562); Thr-749 phosphorylation was critical for dbcAMP-induced Rac1 activation and neurite extension. Bucladesine 113-119 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-3 21460187-9 2011 During dbcAMP-induced neurite outgrowth, PKA activation at the plasma membrane became localized to neurite tips; this localization may contribute to local Rac1 activation at the same neurite tips. Bucladesine 7-13 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 41-44 17960568-6 2008 Treatment with either of the protein kinase A (PKA) inhibitors KT5720 or H-89 followed by exposure to 1 mM DbcAMP for 24 h markedly attenuated DbcAMP-induced alpha-ENaC protein formation and I(SC). Bucladesine 143-149 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 29-45 17960568-6 2008 Treatment with either of the protein kinase A (PKA) inhibitors KT5720 or H-89 followed by exposure to 1 mM DbcAMP for 24 h markedly attenuated DbcAMP-induced alpha-ENaC protein formation and I(SC). Bucladesine 143-149 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 47-50 15571236-2 2004 Dibutyryl cyclic AMP (dbcAMP), forskolin and glucagon, activating glycogen phosphorylase through activation of protein kinase A (PKA), were found to raise PRPP availability by 44%-56%. Bucladesine 0-20 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 111-127 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). Bucladesine 0-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 118-134 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). Bucladesine 0-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 136-139 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). Bucladesine 24-31 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 118-134 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). Bucladesine 24-31 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 136-139 15571236-2 2004 Dibutyryl cyclic AMP (dbcAMP), forskolin and glucagon, activating glycogen phosphorylase through activation of protein kinase A (PKA), were found to raise PRPP availability by 44%-56%. Bucladesine 0-20 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 129-132 15571236-2 2004 Dibutyryl cyclic AMP (dbcAMP), forskolin and glucagon, activating glycogen phosphorylase through activation of protein kinase A (PKA), were found to raise PRPP availability by 44%-56%. Bucladesine 22-28 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 111-127 15571236-2 2004 Dibutyryl cyclic AMP (dbcAMP), forskolin and glucagon, activating glycogen phosphorylase through activation of protein kinase A (PKA), were found to raise PRPP availability by 44%-56%. Bucladesine 22-28 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 129-132 12651935-2 2003 To examine this regulation at the signal transduction level, we treated cultured dental follicle cells with either phorbolmyristate acetate (PMA) or dibutyryl cyclic AMP (dbcAMP) to activate either protein kinase C (PKC) or protein kinase A (PKA). Bucladesine 149-169 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 224-240 15025936-6 2004 In db-cAMP-stimulated cells, inhibition of protein kinase A (PKA) and protein kinase C (PKC) reduced immunolabeling of NOS and concomitantly lowered NO production. Bucladesine 3-10 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 61-64 15025936-6 2004 In db-cAMP-stimulated cells, inhibition of protein kinase A (PKA) and protein kinase C (PKC) reduced immunolabeling of NOS and concomitantly lowered NO production. Bucladesine 3-10 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 43-59 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. Bucladesine 144-150 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 25-41 12651935-2 2003 To examine this regulation at the signal transduction level, we treated cultured dental follicle cells with either phorbolmyristate acetate (PMA) or dibutyryl cyclic AMP (dbcAMP) to activate either protein kinase C (PKC) or protein kinase A (PKA). Bucladesine 171-177 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 242-245 12651935-2 2003 To examine this regulation at the signal transduction level, we treated cultured dental follicle cells with either phorbolmyristate acetate (PMA) or dibutyryl cyclic AMP (dbcAMP) to activate either protein kinase C (PKC) or protein kinase A (PKA). Bucladesine 149-169 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 242-245 12651935-2 2003 To examine this regulation at the signal transduction level, we treated cultured dental follicle cells with either phorbolmyristate acetate (PMA) or dibutyryl cyclic AMP (dbcAMP) to activate either protein kinase C (PKC) or protein kinase A (PKA). Bucladesine 171-177 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 224-240 12099721-4 2002 A pro-apoptotic effect of beta(1)-AR was also blocked by the PKA inhibitor H89, while the protein kinase A (PKA) activators forskolin and dibutyryl-cAMP both induced apoptosis. Bucladesine 138-152 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 90-106 12504778-7 2003 The neuroprotective action of propentofylline was comparably replaced with dibutyryl cAMP (dbcAMP) and was completely suppressed by a low concentration of specific protein kinase A (PKA) inhibitor. Bucladesine 75-89 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 182-185 12504778-7 2003 The neuroprotective action of propentofylline was comparably replaced with dibutyryl cAMP (dbcAMP) and was completely suppressed by a low concentration of specific protein kinase A (PKA) inhibitor. Bucladesine 91-97 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 182-185 12117555-5 2002 The dbcAMP-induced effects on AQP5 and AQP9 mRNAs were inhibited by PKA inhibitors. Bucladesine 4-10 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 68-71 12117555-7 2002 These results suggest that signal transduction via PKA may play important roles in regulating the expression of AQP5 and AQP9, and the effect on AQP9 may be mediated by some factors induced by dbcAMP. Bucladesine 193-199 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 51-54 12099721-4 2002 A pro-apoptotic effect of beta(1)-AR was also blocked by the PKA inhibitor H89, while the protein kinase A (PKA) activators forskolin and dibutyryl-cAMP both induced apoptosis. Bucladesine 138-152 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 108-111 9379405-11 1997 Protein kinase A (PKA) activation with 2.5 mM adenosine 3",5"-cyclic adenosine monophosphate, N6,O2-dibutyryl, sodium salt (db-cAMP) resulted in reduction of INa to 62.8 +/- 5.5% without an effect on activation or steady-state inactivation. Bucladesine 124-131 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-16 11133354-6 2001 Interestingly, application of dibutyryl cAMP (+ 56.2%) or 8-bromo-cAMP (+ 174.7%) significantly increased the occurrence of U50488H-induced Ca(2+) mobilization while protein kinase A (PKA) inhibitors, Rp-cAMP (-32.3%) or myr-psi PKA (-73.9%) significantly reduced the response. Bucladesine 30-44 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 166-182 11133354-6 2001 Interestingly, application of dibutyryl cAMP (+ 56.2%) or 8-bromo-cAMP (+ 174.7%) significantly increased the occurrence of U50488H-induced Ca(2+) mobilization while protein kinase A (PKA) inhibitors, Rp-cAMP (-32.3%) or myr-psi PKA (-73.9%) significantly reduced the response. Bucladesine 30-44 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 184-187 11133354-6 2001 Interestingly, application of dibutyryl cAMP (+ 56.2%) or 8-bromo-cAMP (+ 174.7%) significantly increased the occurrence of U50488H-induced Ca(2+) mobilization while protein kinase A (PKA) inhibitors, Rp-cAMP (-32.3%) or myr-psi PKA (-73.9%) significantly reduced the response. Bucladesine 30-44 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 229-232 10972167-6 2000 Stimulation of PKA activity was also seen with forskolin and di-butyryl cAMP. Bucladesine 61-76 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 15-18 10878598-9 2000 Pretreating cells with PKA inhibitor, H-89, prevented the effect of dibutyryl cAMP. Bucladesine 68-82 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 23-26 9888553-2 1998 The protein kinase A (PKA) pathway agonists forskolin, dibutyryl cAMP and ACTH caused a 5-10 fold increase in 11beta-HSD2 mRNA as determined by semiquantitative PCR. Bucladesine 55-69 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 9888553-2 1998 The protein kinase A (PKA) pathway agonists forskolin, dibutyryl cAMP and ACTH caused a 5-10 fold increase in 11beta-HSD2 mRNA as determined by semiquantitative PCR. Bucladesine 55-69 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 9379405-11 1997 Protein kinase A (PKA) activation with 2.5 mM adenosine 3",5"-cyclic adenosine monophosphate, N6,O2-dibutyryl, sodium salt (db-cAMP) resulted in reduction of INa to 62.8 +/- 5.5% without an effect on activation or steady-state inactivation. Bucladesine 124-131 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 18-21 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. Bucladesine 143-149 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 4-20 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. Bucladesine 143-149 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 22-25 9275048-12 1997 These studies indicate that forskolin and dbcAMP stimulate PLD in FRTL-5 thyroid cells directly via PKA without involvement of PKC. Bucladesine 42-48 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 100-103 9236220-4 1997 PKA was induced by perfusing oocytes with a cocktail that contained forskolin, chlorophenylthio-cAMP, dibutyryl-cAMP, and 3-isobutyl-1-methylxanthine. Bucladesine 102-116 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-3 2023931-2 1991 32P-radiolabeling of rat glioma C6 cells revealed plectin as a major in vivo target of protein kinase A and protein kinase C. Plectin, present in lysates of dibutyryladenosine 3",5"-cyclic monophosphate-treated cells, showed a 2.5 times higher binding affinity to vimentin than plectin from phorbol ester-treated cells. Bucladesine 157-202 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 87-103 9054858-6 1997 Similar synergistic activation of MAP kinases was observed when other protein kinase A-activating agents such as forskolin, dibutyryl cAMP, and isobutyl-methylxanthine were used with a protein kinase C-activating agent at the same time. Bucladesine 124-138 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 70-86 8410184-4 1993 Activation of protein kinase A (PKA) with dibutyryl-cAMP also protected during ischemia, although it was not additive with the effect provided by growth factors. Bucladesine 42-56 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 14-30 8410184-4 1993 Activation of protein kinase A (PKA) with dibutyryl-cAMP also protected during ischemia, although it was not additive with the effect provided by growth factors. Bucladesine 42-56 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 32-35 34721684-13 2021 Treatment with bucladesine, a selective PKA agonist, partially reversed the deleterious effects of Sev. Bucladesine 15-26 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 40-43 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. Bucladesine 127-138 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 107-110 35261620-0 2022 Melatonin alleviates traumatic brain injury-induced anxiety-like behaviors in rats: Roles of the protein kinase A/cAMP-response element binding signaling pathway. Bucladesine 114-118 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 97-113 35261620-7 2022 H89 (0.02 mg/kg), a special protein kinase A (PKA) inhibitor, or dibutyryl-cyclic adenosine monophosphate (cAMP; 0.1 mg/kg), an activator of PKA, were administered by stereotactic injection of the brain to evaluate the roles of PKA and cAMP-response element-binding protein (CREB) in melatonin-related mood regulation, respectively. Bucladesine 107-111 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 141-144 33447972-8 2021 However, lipolysis stimulated by dibutyryl-cAMP (a direct activator of protein kinase A) and the antilipolytic action of insulin were not affected by BPA. Bucladesine 33-47 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 71-87 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. Bucladesine 215-229 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 201-204 28222740-13 2017 Db-cAMP increased phosphorylated cAMP-response element-binding protein (p-CREB) via protein kinase A (PKA) signaling, and decreased nuclear p-Smad2/3 binding with CREB binding protein (CBP), which reduced activation of p-Smads in fibroblasts induced by Ang II. Bucladesine 0-7 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 84-100 28222740-13 2017 Db-cAMP increased phosphorylated cAMP-response element-binding protein (p-CREB) via protein kinase A (PKA) signaling, and decreased nuclear p-Smad2/3 binding with CREB binding protein (CBP), which reduced activation of p-Smads in fibroblasts induced by Ang II. Bucladesine 0-7 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 102-105 28222740-14 2017 CONCLUSIONS: This study showed an anti-silicotic effect of db-cAMP that was mediated via PKA/p-CREB/CBP signaling. Bucladesine 59-66 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 89-92