PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24886333-9	2014	Functional diversity was observed between clonal populations with 10 muM isoproterenol-induced cyclic AMP responses ranging from 1.4 - 5.4 fold cf basal and bradykinin-induced inositol phosphate from 1.8 - 5.2 fold cf basal.	Cyclic AMP	95-105	kininogen 1	Homo sapiens	157-167	
25505603-8	2014	As in the EP1 experiments, expression of PGT at the plasma membrane caused a reduction in bradykinin-induced cAMP accumulation.	Cyclic AMP	109-113	kininogen 1	Homo sapiens	90-100	
20082561-0	2010	Evidence for prostacyclin and cAMP upregulation by bradykinin and insulin-like growth factor 1 in vascular smooth muscle cells.	Cyclic AMP	30-34	kininogen 1	Homo sapiens	51-61	
23796753-6	2013	In preadipocytes, BK also induced a rapid and transient [Ca2+](i) mobilization, a rapid and sustained increase in ERK1/2 activation and enhanced forskolin-stimulated cAMP accumulation.	Cyclic AMP	166-170	kininogen 1	Homo sapiens	18-20	
20584115-12	2011	The relaxing effects of VIP and BK were paralleled by a 4.8-fold and fivefold increase in cAMP, while the production of cGMP was stimulated 38-fold and 119-fold in the presence of CNP or BK, respectively.	Cyclic AMP	90-94	kininogen 1	Homo sapiens	32-34	
20082561-3	2010	Activation of BK or IGF-1 receptors stimulated the synthesis and release of prostacyclin (PGI(2)) leading to increased production of cAMP in VSMC.	Cyclic AMP	133-137	kininogen 1	Homo sapiens	14-16	
20082561-4	2010	Inhibition of p42/p44(mapk) or src kinases prevented the increase in PGI(2) and cAMP observed in response to BK or IGF-1, indicating a role for these kinases in the regulation of cPLA(2) activity in the VSMC.	Cyclic AMP	80-84	kininogen 1	Homo sapiens	109-111	
19145781-16	2009	CONCLUSION: Our results demonstrate that bradykinin regulates TRPM7 and its downstream target annexin-1 through phospholipase C-dependent, protein kinase C-dependent and c-Src-dependent and cAMP-independent pathways; effects are mediated through bradykinin type 2 receptor; and bradykinin regulates VSMC [Mg2+]i and migration through TRPM7.	Cyclic AMP	190-194	kininogen 1	Homo sapiens	41-51	
19145781-3	2009	METHODS: Here, we tested the hypothesis that bradykinin and its second messenger cAMP upregulate TRPM7, which stimulates activation of annexin-1 (TRPM7 substrate) and increases transmembrane Mg2+ transport and vascular smooth muscle cell (VSMC) migration.	Cyclic AMP	81-85	kininogen 1	Homo sapiens	45-55	
19788733-3	2009	Here we study the role of the cyclic AMP (cAMP) effectors protein kinase A (PKA) and exchange proteins directly activated by cAMP (Epac1 and Epac2) in the bradykinin-induced IL-8 release from a human airway smooth muscle cell line and the underlying molecular mechanisms of this response.	Cyclic AMP	30-40	kininogen 1	Homo sapiens	155-165	
19788733-3	2009	Here we study the role of the cyclic AMP (cAMP) effectors protein kinase A (PKA) and exchange proteins directly activated by cAMP (Epac1 and Epac2) in the bradykinin-induced IL-8 release from a human airway smooth muscle cell line and the underlying molecular mechanisms of this response.	Cyclic AMP	42-46	kininogen 1	Homo sapiens	155-165	
19788733-3	2009	Here we study the role of the cyclic AMP (cAMP) effectors protein kinase A (PKA) and exchange proteins directly activated by cAMP (Epac1 and Epac2) in the bradykinin-induced IL-8 release from a human airway smooth muscle cell line and the underlying molecular mechanisms of this response.	Cyclic AMP	125-129	kininogen 1	Homo sapiens	155-165	
19788733-12	2009	The PKA activator 6-Bnz-cAMP and the Epac activator 8-pCPT-2"-O-Me-cAMP significantly increased bradykinin-induced IL-8 release.	Cyclic AMP	24-28	kininogen 1	Homo sapiens	96-106	
17047985-5	2006	The two phases can be assigned to second messengers of the BK-signalling pathway: Ca(2+) for the decrease and cyclic adenosine monophosphate for the rise of resistance, respectively.	Cyclic AMP	110-140	kininogen 1	Homo sapiens	59-61	
18156442-0	2008	IL-1beta, BK, and TGF-beta1 attenuate PGI2-mediated cAMP formation in human pulmonary artery smooth muscle cells by multiple mechanisms involving p38 MAP kinase and PKA.	Cyclic AMP	52-56	kininogen 1	Homo sapiens	10-12	
18156442-1	2008	We have previously shown that interleukin (IL)-1beta, transforming growth factor (TGF)-beta1, or bradykinin (BK) impair cAMP generation in response to prostacyclin analogs in human pulmonary artery smooth muscle (PASM), suggesting that inflammation can impair the effects of prostacyclin analogs on PASM in pulmonary hypertension.	Cyclic AMP	120-124	kininogen 1	Homo sapiens	97-107	
18156442-1	2008	We have previously shown that interleukin (IL)-1beta, transforming growth factor (TGF)-beta1, or bradykinin (BK) impair cAMP generation in response to prostacyclin analogs in human pulmonary artery smooth muscle (PASM), suggesting that inflammation can impair the effects of prostacyclin analogs on PASM in pulmonary hypertension.	Cyclic AMP	120-124	kininogen 1	Homo sapiens	109-111	
18156442-7	2008	These studies suggest that IL-1beta, BK, and TGF-beta1 impair IP receptor-mediated cAMP accumulation by multiple effects on different components of the signaling pathway and that these effects are PKA and p38 MAP kinase dependent.	Cyclic AMP	83-87	kininogen 1	Homo sapiens	37-39	
16093449-0	2005	Bradykinin signaling counteracts cAMP-elicited aquaporin 2 translocation in renal cells.	Cyclic AMP	33-37	kininogen 1	Homo sapiens	0-10	
15050422-0	2004	Cyclic AMP increases bradykinin receptor binding affinity in human endothelial cells.	Cyclic AMP	0-10	kininogen 1	Homo sapiens	21-31	
15911880-4	2005	The IP(3)R complex functions as a focal point to promote Ca(2+) release in two ways: (1) it facilitates PKA-dependent phosphorylation of IP(3)R1 in response to BK-induced elevation of cAMP, and (2) it couples the plasmalemmal EGFR with IP(3)R1 at the Ca(2+) store located juxtaposed to the plasma membrane.	Cyclic AMP	184-188	kininogen 1	Homo sapiens	160-162	
15050422-1	2004	We demonstrated bradykinin receptors in human endothelial cells and studied whether bradykinin receptors might be regulated by cyclic AMP.	Cyclic AMP	127-137	kininogen 1	Homo sapiens	84-94	
15050422-9	2004	These results suggest, that the dibutyryl-cAMP stimulated increase in (125)I-[Tyr(8)]-bradykinin binding is probably due to increased B(1) receptor affinity with no change in receptor capacity.	Cyclic AMP	42-46	kininogen 1	Homo sapiens	86-96	
14670842-0	2004	Interleukin-1beta, transforming growth factor-beta1, and bradykinin attenuate cyclic AMP production by human pulmonary artery smooth muscle cells in response to prostacyclin analogues and prostaglandin E2 by cyclooxygenase-2 induction and downregulation of adenylyl cyclase isoforms 1, 2, and 4.	Cyclic AMP	78-88	kininogen 1	Homo sapiens	57-67	
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Cyclic AMP	167-171	kininogen 1	Homo sapiens	54-64	
14670842-6	2004	The effect of IL-1beta, BK, and TGF-beta1 on cAMP levels was abrogated by the selective COX-2 inhibitor NS398.	Cyclic AMP	45-49	kininogen 1	Homo sapiens	24-26	
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Cyclic AMP	167-171	kininogen 1	Homo sapiens	66-68	
14517215-9	2003	CRE activation occurred by BK inducing cytosolic phospholipase A2-mediated arachidonic acid release and rapid prostaglandin E2 (PGE2) production, thereby increasing cAMP.	Cyclic AMP	165-169	kininogen 1	Homo sapiens	27-29	
14517215-10	2003	Indomethacin inhibited BK-induced PGE2 production, cAMP accumulation, and CRE/luc reporter and COX-2 promoter luciferase activity.	Cyclic AMP	51-55	kininogen 1	Homo sapiens	23-25	
14517215-0	2003	Cyclooxygenase-2 induction by bradykinin in human pulmonary artery smooth muscle cells is mediated by the cyclic AMP response element through a novel autocrine loop involving endogenous prostaglandin E2, E-prostanoid 2 (EP2), and EP4 receptors.	Cyclic AMP	106-116	kininogen 1	Homo sapiens	30-40	
14645533-3	2003	By transfection with various COX-2 promoter reporter constructs, we found that the bp -327-to-+59 promoter region was essential for COX-2 gene transcription by bradykinin and IL-1beta and that the cyclic AMP response element (CRE) was critical in bradykinin-induced transcription, whereas nuclear factor IL-6 and CRE and, to a lesser extent, nuclear factor-kappaB (NF-kappaB) were involved in IL-1beta-induced transcription.	Cyclic AMP	197-207	kininogen 1	Homo sapiens	160-170	
14645533-3	2003	By transfection with various COX-2 promoter reporter constructs, we found that the bp -327-to-+59 promoter region was essential for COX-2 gene transcription by bradykinin and IL-1beta and that the cyclic AMP response element (CRE) was critical in bradykinin-induced transcription, whereas nuclear factor IL-6 and CRE and, to a lesser extent, nuclear factor-kappaB (NF-kappaB) were involved in IL-1beta-induced transcription.	Cyclic AMP	197-207	kininogen 1	Homo sapiens	247-257	
7998998-10	1994	Deoxyadenosine (0.1 mM), a P-site inhibitor of adenylate cyclase, blocked bradykinin-stimulated cyclic AMP formation and converted the activation of ERK-2 into a sustained response.	Cyclic AMP	96-106	kininogen 1	Homo sapiens	74-84	
11164180-10	2001	The relaxing potency of BK was paralleled by its ability to elevate the intracellular levels of cAMP and cGMP.	Cyclic AMP	96-100	kininogen 1	Homo sapiens	24-26	
10370087-14	1999	In conclusion, BK enhances cyclic adenosine monophosphate-stimulated Cl- secretion in T84 cells, probably via basolateral, Ca2+-liganded activation of low-conductance hSK4-type K+ channels.	Cyclic AMP	27-57	kininogen 1	Homo sapiens	15-17	
10199815-10	1999	Priming with PGE2 (10(-8)-10(-6) M) over 24 h mimicked the effect of TGF-alpha on bradykinin-induced changes in cAMP and SCC.	Cyclic AMP	112-116	kininogen 1	Homo sapiens	82-92	
9700093-0	1998	Impaired cAMP production in human airway smooth muscle cells by bradykinin: role of cyclooxygenase products.	Cyclic AMP	9-13	kininogen 1	Homo sapiens	64-74	
9475508-4	1998	ATP, histamine, bradykinin, and serotonin significantly decreased model BBB transendothelial electrical resistance and manipulations which elevate cyclic AMP enhanced culture resistance.	Cyclic AMP	147-157	kininogen 1	Homo sapiens	16-26	
8890934-4	1996	The inhibition by CTX appeared to be secondary to its ability to increase cyclic AMP, because forskolin also inhibited the BK-mediated Ins (1,4,5)P3 release.	Cyclic AMP	74-84	kininogen 1	Homo sapiens	123-125	
7702566-3	1995	Therefore, activation of Gs (by cholera-toxin pre-treatment) amplified the bradykinin-stimulated cyclic AMP signal and concurrently attenuated the partial activation of extracellular-signal-regulated kinase-2 (ERK-2) by bradykinin.	Cyclic AMP	97-107	kininogen 1	Homo sapiens	75-85	
7702566-4	1995	We have previously demonstrated that, in order to induce full activation of ERK-2 with bradykinin, it is necessary to obliterate PKC-stimulated cyclic AMP formation.	Cyclic AMP	144-154	kininogen 1	Homo sapiens	87-97	
7702566-8	1995	The present study indicates that the bradykinin-stimulated ERK-2 pathway is entirely cyclic AMP-sensitive, and suggests that coincident signal detection by adenylate cyclase may be an important physiological route for the modulation of early mitogenic signalling.	Cyclic AMP	85-95	kininogen 1	Homo sapiens	37-47	
9371732-0	1997	Bradykinin stimulates cAMP synthesis via mitogen-activated protein kinase-dependent regulation of cytosolic phospholipase A2 and prostaglandin E2 release in airway smooth muscle.	Cyclic AMP	22-26	kininogen 1	Homo sapiens	0-10	
9371732-1	1997	Bradykinin stimulates cAMP synthesis in cultured airway smooth muscle (ASM) cells.	Cyclic AMP	22-26	kininogen 1	Homo sapiens	0-10	
8940106-0	1996	Tyrosine phosphorylation of GSalpha and inhibition of bradykinin-induced activation of the cyclic AMP pathway in A431 cells by epidermal growth factor receptor.	Cyclic AMP	91-101	kininogen 1	Homo sapiens	54-64	
8940106-2	1996	In a previous study, we demonstrated that bradykinin (BK) increases the intracellular accumulation of cAMP in the human epidermoid carcinoma cell line A431 by stimulating adenylate cyclase activity via a stimulatory G protein (Gsalpha) (Liebmann, C., Graness, A., Ludwig, B., Adomeit, A., Boehmer, A., Boehmer, F.-D., Nurnberg, B., and Wetzker, R. (1996) Biochem.	Cyclic AMP	102-106	kininogen 1	Homo sapiens	42-52	
8940106-2	1996	In a previous study, we demonstrated that bradykinin (BK) increases the intracellular accumulation of cAMP in the human epidermoid carcinoma cell line A431 by stimulating adenylate cyclase activity via a stimulatory G protein (Gsalpha) (Liebmann, C., Graness, A., Ludwig, B., Adomeit, A., Boehmer, A., Boehmer, F.-D., Nurnberg, B., and Wetzker, R. (1996) Biochem.	Cyclic AMP	102-106	kininogen 1	Homo sapiens	54-56	
8940106-5	1996	Here, we present several lines of evidence indicating the ability of epidermal growth factor (EGF) to suppress BK-induced activation of the cAMP pathway in A431 cells via tyrosine phosphorylation of Gsalpha.	Cyclic AMP	140-144	kininogen 1	Homo sapiens	111-113	
8940106-10	1996	Treatment of A431 cells with EGF decreased BK-induced cAMP accumulation in intact cells as well as the stimulation of adenylate cyclase by BK, NaF, and guanyl nucleotides, but not by forskolin.	Cyclic AMP	54-58	kininogen 1	Homo sapiens	43-45	
8833191-0	1996	Potentiation of bradykinin-induced inositol phosphates production by cyclic AMP elevating agents and endothelin-1 in cultured astrocytes.	Cyclic AMP	69-79	kininogen 1	Homo sapiens	16-26	
7998998-11	1994	Thus the PKC-stimulated cyclic AMP response can limit the activation of ERK-2 in response to bradykinin.	Cyclic AMP	24-34	kininogen 1	Homo sapiens	93-103	
8040274-8	1994	Consequently, in bradykinin-stimulated cells, the adenylyl cyclase system regulates Ca influx through cAMP-dependent protein kinase, but not intracellular Ca release.	Cyclic AMP	102-106	kininogen 1	Homo sapiens	17-27	
8132619-1	1994	Neuropeptide Y (NPY) attenuated angiotensin II (AII)-or bradykinin (BK)-induced Ca2+ release from intracellular stores and inhibited forskolin-stimulated cAMP accumulation and omega-conotoxin-sensitive high K(+)-induced Ca2+ influx in the human neuroblastoma cell line SMS-KAN. All three NPY actions were mediated via Y2 receptors.	Cyclic AMP	154-158	kininogen 1	Homo sapiens	56-66	
7950978-3	1994	Bradykinin causes a rapid decrease in A2B receptor mediated cAMP formation, via a mechanism that involves calcium, but not cGMP, and appears to depend upon a direct decrease in adenylyl cyclase.	Cyclic AMP	60-64	kininogen 1	Homo sapiens	0-10	
8200990-0	1994	Cyclic AMP selectively enhances bradykinin receptor synthesis and expression in cultured arterial smooth muscle.	Cyclic AMP	0-10	kininogen 1	Homo sapiens	32-42	
8200990-4	1994	Short term stimulation (1 min) with cyclic AMP produced a variable inhibition of bradykinin-stimulated calcium mobilization which was lost in later passaged cells.	Cyclic AMP	36-46	kininogen 1	Homo sapiens	81-91	
8200990-6	1994	Further analysis demonstrated that chronic exposure to cAMP produced a twofold increase in both the number of cell surface bradykinin receptors and in bradykinin-stimulated phosphoinositide hydrolysis.	Cyclic AMP	55-59	kininogen 1	Homo sapiens	123-133	
8200990-6	1994	Further analysis demonstrated that chronic exposure to cAMP produced a twofold increase in both the number of cell surface bradykinin receptors and in bradykinin-stimulated phosphoinositide hydrolysis.	Cyclic AMP	55-59	kininogen 1	Homo sapiens	151-161	
8200990-7	1994	The increase in bradykinin receptors was time dependent (> 7 h) and blocked by protein synthesis inhibitors, suggesting that cAMP enhanced the synthesis of new bradykinin receptors.	Cyclic AMP	128-132	kininogen 1	Homo sapiens	16-26	
8200990-7	1994	The increase in bradykinin receptors was time dependent (> 7 h) and blocked by protein synthesis inhibitors, suggesting that cAMP enhanced the synthesis of new bradykinin receptors.	Cyclic AMP	128-132	kininogen 1	Homo sapiens	163-173	
8200990-10	1994	In summary, prolonged treatment with cAMP selectively stimulates the synthesis and expression of bradykinin receptors on arterial smooth muscle while decreasing the responsiveness to vasoconstrictor agonists such as angiotensin II and vasopressin.	Cyclic AMP	37-41	kininogen 1	Homo sapiens	97-107	
8206319-4	1994	On the contrary, pretreatment with IGF-II for 10 min enhanced the cAMP production stimulated by bradykinin (10 nM, 3 min) by 2.5-fold whereas no additive effects of IGF-II on the increased ligand binding to the mannose 6-phosphate/IGF-II receptor in response to bradykinin were observed.	Cyclic AMP	66-70	kininogen 1	Homo sapiens	96-106	
7688545-0	1993	Bradykinin inhibits cyclic AMP accumulation in D384-human astrocytoma cells via a calcium-dependent inhibition of adenylyl cyclase.	Cyclic AMP	20-30	kininogen 1	Homo sapiens	0-10	
7688545-9	1993	Bradykinin treatment, which attenuates cAMP accumulation in intact cells, did not do so in plasma membranes.	Cyclic AMP	39-43	kininogen 1	Homo sapiens	0-10	
7688545-10	1993	These findings suggest that bradykinin-induced inhibition of cAMP formation in D384 cells requires mobilization of [Ca2+]i and subsequent entry of Ca2+ which directly interacts with a component of the adenylyl cyclase system.	Cyclic AMP	61-65	kininogen 1	Homo sapiens	28-38	
7688545-1	1993	Bradykinin causes a concentration-dependent, transient rise in intracellular Ca2+ and a sustained inhibition of forskolin-, dopamine- and 5"-N-ethyl-carboxamidoadenosine (NECA)-stimulated cAMP accumulation in D384 astrocytoma cells.	Cyclic AMP	188-192	kininogen 1	Homo sapiens	0-10	
7688545-2	1993	Chelation of intracellular calcium abolished bradykinin"s inhibitory effect on cAMP accumulation.	Cyclic AMP	79-83	kininogen 1	Homo sapiens	45-55	
1284620-0	1992	Bradykinin inhibition of cyclic AMP accumulation in D384 astrocytoma cells.	Cyclic AMP	25-35	kininogen 1	Homo sapiens	0-10	
1330642-2	1992	Maximal amplitude and duration of cyclic GMP response to bradykinin were about 2-fold greater in cells with cyclic AMP levels increased by forskolin pretreatment than in control cells with basal levels of cyclic AMP.	Cyclic AMP	108-118	kininogen 1	Homo sapiens	57-67	
1330642-2	1992	Maximal amplitude and duration of cyclic GMP response to bradykinin were about 2-fold greater in cells with cyclic AMP levels increased by forskolin pretreatment than in control cells with basal levels of cyclic AMP.	Cyclic AMP	205-215	kininogen 1	Homo sapiens	57-67	
1284620-7	1992	The inhibitory effect of nitroprusside was totally reversed by blocking the soluble guanylate cyclase activity by methylene blue treatment; however, the inhibitory action of bradykinin on cAMP accumulation was not changed by this treatment.	Cyclic AMP	188-192	kininogen 1	Homo sapiens	174-184	
1328896-8	1992	Bradykinin was also found to attenuate dopamine stimulated cyclic AMP accumulation in D384 cells, at similar concentrations previously observed to stimulate the phospholipase C signal transduction pathway, in the presence of the phosphodiesterase inhibitor, rolipram.	Cyclic AMP	59-69	kininogen 1	Homo sapiens	0-10	
1284620-2	1992	The present studies were performed in order to examine the possible role of cyclic GMP-stimulated phosphodiesterase (cGMP-PDE) activity in the inhibitory action of the inflammatory peptide bradykinin on cyclic AMP (cAMP) accumulation in D384 cells.	Cyclic AMP	203-213	kininogen 1	Homo sapiens	189-199	
1284620-2	1992	The present studies were performed in order to examine the possible role of cyclic GMP-stimulated phosphodiesterase (cGMP-PDE) activity in the inhibitory action of the inflammatory peptide bradykinin on cyclic AMP (cAMP) accumulation in D384 cells.	Cyclic AMP	215-219	kininogen 1	Homo sapiens	189-199	
1284620-3	1992	Bradykinin decreased the forskolin-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor rolipram, and caused a transient 50% rise in cellular cGMP in the presence of the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine (IBMX).	Cyclic AMP	46-50	kininogen 1	Homo sapiens	0-10	
1317654-10	1992	By contrast, nanomolar concentrations of bradykinin, which increases Ca(2+)-levels and protein kinase C activity in D384 cells, reduced NECA-induced cyclic AMP accumulation in control and pertussis toxin-treated cells.	Cyclic AMP	149-159	kininogen 1	Homo sapiens	41-51	
1330055-1	1992	Recombinant human interleukin-1 beta (IL-1 beta) and bradykinin (BK) synergistically stimulate prostaglandin E2 (PGE2) formation in human gingival fibroblasts cultured for 24 h. Neither BK or IL-1 beta per se, nor their combinations, caused any acute stimulation of cellular cyclic AMP accumulation.	Cyclic AMP	275-285	kininogen 1	Homo sapiens	53-63	
1330055-1	1992	Recombinant human interleukin-1 beta (IL-1 beta) and bradykinin (BK) synergistically stimulate prostaglandin E2 (PGE2) formation in human gingival fibroblasts cultured for 24 h. Neither BK or IL-1 beta per se, nor their combinations, caused any acute stimulation of cellular cyclic AMP accumulation.	Cyclic AMP	275-285	kininogen 1	Homo sapiens	65-67	
1767868-9	1991	The reduced responses of CF cells to bradykinin and methacholine, in addition to isoproterenol, suggest that both Ca-dependent and adenosine 3",5"-cyclic monophosphate-dependent regulation of Cl secretion are defective in CF tracheobronchial glands.	Cyclic AMP	131-167	kininogen 1	Homo sapiens	37-47	
3018483-9	1986	NP caused a small, early increase in cAMP without significant effect on prostaglandin I2 (PGI2); after 2.5 min, effects on PGI2 and cAMP were greater with BK and NP than with BK alone.	Cyclic AMP	132-136	kininogen 1	Homo sapiens	155-157	
1845801-1	1991	The possible role of cAMP and/or arachidonic acid (and metabolites) in the stimulation of glucose transport elicited by bradykinin in Swiss 3T3 fibroblasts was investigated with particular attention to the part of this effect inhibitable by pertussis toxin.	Cyclic AMP	21-25	kininogen 1	Homo sapiens	120-130	
2843748-5	1988	Agents such as cholera toxin, which elevated cAMP, also increased bradykinin-induced prostaglandin production.	Cyclic AMP	45-49	kininogen 1	Homo sapiens	66-76	
2843748-6	1988	These data are consistent with the hypothesis that the enhanced sensitivity to bradykinin after pertussis toxin treatment results from modification of Gi alpha and increased cAMP, leading to enhanced formation of prostaglandins in response to bradykinin.	Cyclic AMP	174-178	kininogen 1	Homo sapiens	79-89	
2843748-6	1988	These data are consistent with the hypothesis that the enhanced sensitivity to bradykinin after pertussis toxin treatment results from modification of Gi alpha and increased cAMP, leading to enhanced formation of prostaglandins in response to bradykinin.	Cyclic AMP	174-178	kininogen 1	Homo sapiens	243-253	
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Cyclic AMP	202-206	kininogen 1	Homo sapiens	95-105	
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Cyclic AMP	202-206	kininogen 1	Homo sapiens	107-109	
3018483-8	1986	BK increased prostaglandin production by the fibroblasts; it is believed that the kinin-induced elevation in cAMP content is secondary to increased prostaglandin formation.	Cyclic AMP	109-113	kininogen 1	Homo sapiens	0-2	
1697359-2	1990	Specific bradykinin (BK) receptor sites (B2 subtype) were measured by direct binding study and correlated with BK-induced biological effects such as the release of inositol phosphates, formation of prostacyclin (PGI2), and accumulation of cyclic 3"5" adenosine monophosphate (cAMP).	Cyclic AMP	276-280	kininogen 1	Homo sapiens	9-19	
1697359-8	1990	Compounds or drugs that enhance intracellular cAMP levels or inhibit generation of eicosanoids were shown to modify the BK response by indirect means.	Cyclic AMP	46-50	kininogen 1	Homo sapiens	120-122	
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	Cyclic AMP	13-17	kininogen 1	Homo sapiens	31-33	
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	Cyclic AMP	13-17	kininogen 1	Homo sapiens	37-39	
3018483-12	1986	These effects of BK or BK plus NP on cAMP thus appear to be mediated through cyclooxygenase products of arachidonate metabolism.	Cyclic AMP	37-41	kininogen 1	Homo sapiens	17-19	
3018483-12	1986	These effects of BK or BK plus NP on cAMP thus appear to be mediated through cyclooxygenase products of arachidonate metabolism.	Cyclic AMP	37-41	kininogen 1	Homo sapiens	23-25	
3004657-3	1986	Bradykinin, alpha-melanocyte-stimulating (alpha-MSH), luteinizing hormone-releasing hormone (LH-RH), oxytocin and carbamylcholine stimulated cAMP accumulation selectively in one or two of the above structures.	Cyclic AMP	141-145	kininogen 1	Homo sapiens	0-10	
225265-0	1979	Regulation of bradykinin-induced cyclic amp response by quinacrine and prostaglandin E2 and F2 alpha in human synovial fibroblasts.	Cyclic AMP	33-43	kininogen 1	Homo sapiens	14-24	
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Cyclic AMP	192-202	kininogen 1	Homo sapiens	19-29	
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Cyclic AMP	192-202	kininogen 1	Homo sapiens	31-33	
6302691-0	1983	Bradykinin stimulates phospholipid methylation, calcium influx, prostaglandin formation, and cAMP accumulation in human fibroblasts.	Cyclic AMP	93-97	kininogen 1	Homo sapiens	0-10	
6302691-1	1983	The biochemical events that lead to bradykinin stimulation of cAMP accumulation in human fibroblasts were examined.	Cyclic AMP	62-66	kininogen 1	Homo sapiens	36-46	
6302691-2	1983	Treatment of human fibroblasts with bradykinin increases phospholipid methylation, Ca2+ influx, arachidonic acid release, prostaglandin formation, and cAMP content.	Cyclic AMP	151-155	kininogen 1	Homo sapiens	36-46	
6302691-6	1983	3-Deazaadenosine, a methyltransferase inhibitor, almost completely inhibited bradykinin-stimulated phospholipid methylation and Ca2+ influx and partially reduced arachidonic acid release and prostaglandin formation but had no effect on cAMP formation.	Cyclic AMP	236-240	kininogen 1	Homo sapiens	77-87	
6302691-7	1983	Mepacrine, a phospholipase inhibitor, blocked bradykinin-induced arachidonic acid release, prostaglandin release, and cAMP accumulation.	Cyclic AMP	118-122	kininogen 1	Homo sapiens	46-56	
6302691-8	1983	Indomethacin, a cyclooxygenase inhibitor, blocked the effect of bradykinin on cAMP accumulation.	Cyclic AMP	78-82	kininogen 1	Homo sapiens	64-74	
6302691-10	1983	These observations indicate that bradykinin generates cAMP via arachidonic acid release and subsequent formation of prostaglandins.	Cyclic AMP	54-58	kininogen 1	Homo sapiens	33-43	
6184749-4	1982	Bradykinin treatment of RPCT cells caused an accumulation of intracellular cAMP which was blocked by aspirin and was quantitatively similar to that observed with 10(-5) M PGE2.	Cyclic AMP	75-79	kininogen 1	Homo sapiens	0-10	
6184749-7	1982	However, at higher concentrations of PGs (e.g. 10(-5) M), the effects of AVP plus PGE1, PGE2, PGI2 or bradykinin on intracellular cAMP levels were not additive.	Cyclic AMP	130-134	kininogen 1	Homo sapiens	102-112	
225265-3	1979	The cyclic AMP response of human synovial fibroblasts to bradykinin is potentiated by prostaglandin E2 and inhibited by prostaglandin F2 alpha.	Cyclic AMP	4-14	kininogen 1	Homo sapiens	57-67	
225265-1	1979	Bradykinin induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the release of [3H]arachidonic acid and [3H]-E prostaglandins from human synovial fibroblasts pre-labeled in their phospholipids.	Cyclic AMP	49-59	kininogen 1	Homo sapiens	0-10	
204962-2	1978	Fetal calf serum in the media also stimulates the synthesis and release of these labeled lipids from pre-labeled human synovial fibroblasts and potentiates the bradykinin-induced cyclic AMP response.	Cyclic AMP	179-189	kininogen 1	Homo sapiens	160-170	
204962-3	1978	The PGE1 analogue, 7-oxa-13 prostynoic acid, completely abrogates both the bradykinin-induced cyclic AMP response and the bradykinin- and fetal calf serum-evoked release of labeled E-prostaglandins from pre-labeled cells.	Cyclic AMP	94-104	kininogen 1	Homo sapiens	75-85	
197839-9	1977	Indomethacin (IM) inhibits the BK evoked cyclic AMP response unless cell cultures are pretreated with PGE1.	Cyclic AMP	41-51	kininogen 1	Homo sapiens	31-33	
197839-10	1977	The PGE1 analog, 7-oxa-13-prostynoic acid, is a better inhibitor of the cyclic AMP response induced by BK than by PGE1.	Cyclic AMP	72-82	kininogen 1	Homo sapiens	103-105	
197839-11	1977	BK does not elicit a cyclic AMP response solely by elaborating PGE1, yet the prostaglandin pathway and its products seem to have a role in the degree of the cyclic AMP response to BK challenge.	Cyclic AMP	157-167	kininogen 1	Homo sapiens	180-182	
172888-2	1975	Agonist that cause contraction (bradykinin, histamine, and serotonin) cause accumulation of guanosine 3":5"-monophosphate (cGMP) without altering adenosine 3":5"-monophosphate (cAMP).	Cyclic AMP	177-181	kininogen 1	Homo sapiens	32-42	
4314857-0	1970	Cyclic AMP mediation of bradykinin-induced stimulation of mitotic activity and DNA synthesis in thymocytes.	Cyclic AMP	0-10	kininogen 1	Homo sapiens	24-34	
31550055-14	2020	Bradykinin-induced bradykinin-2-receptor signaling through intracellular calcium mobilization and reduction in cAMP levels, triggered changes in solute permeability and cellular junction expression.	Cyclic AMP	111-115	kininogen 1	Homo sapiens	0-10	
204962-1	1978	Bradykinin, a potent inflammatory mediator, induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the synthesis and release of 3H-arachidonic acid and 3H-E prostaglandins from these cells pre-labeled in their phospholipids.	Cyclic AMP	82-92	kininogen 1	Homo sapiens	0-10	
197839-1	1977	Human synovial fibroblasts in culture respond to bradykinin (8 X 10(-9) M) with an increment in intracellular cyclic AMP concentration.	Cyclic AMP	110-120	kininogen 1	Homo sapiens	49-59	
197839-3	1977	The cyclic AMP response to BK is enhanced by a heat stable factor(s) in fetal calf serum (FCS) and by the addition of arachidonic acid (AA) to monolayer cultures incubated in serum-free media.	Cyclic AMP	4-14	kininogen 1	Homo sapiens	27-29	
197839-5	1977	These BK refractory cells do respond with significant increment in cyclic AMP to challenge with prostaglandin E1 (PGE1).	Cyclic AMP	67-77	kininogen 1	Homo sapiens	6-8	
197839-8	1977	When both BK and PGE1 are incubated together with synovial fibroblasts, the cyclic AMP response elicited is more than additive as compared to the response of each hormone separately.	Cyclic AMP	76-86	kininogen 1	Homo sapiens	10-12	
191875-1	1977	Human synovial fibroblasts in culture respond to bradykinin with a 20-fold increment in intracellular cyclic AMP concentrations, however bradykinin does not directly activate adenylate cyclase activity in a particulate fraction derived from these cells.	Cyclic AMP	102-112	kininogen 1	Homo sapiens	49-59	
191875-3	1977	Hydrocortisone inhibits the bradykinin induced increment in cyclic AMP and the release of arachidonic acid and prostaglandins E and F from synovial fibroblasts.	Cyclic AMP	60-70	kininogen 1	Homo sapiens	28-38	
191875-4	1977	Indomethacin, which also inhibits the cyclic AMP response to bradykinin, has no effect on the release of arachidonic acid from synovial fibroblasts.	Cyclic AMP	38-48	kininogen 1	Homo sapiens	61-71