PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19855060-1 2010 Nitric oxide (NO), synthesized by endothelial nitric oxide synthase (eNOS), exerts control over vascular function via two distinct mechanisms, the activation of soluble guanylate cyclase (sGC)/cGMP-dependent signaling or through S-nitrosylation of proteins with reactive thiols (S-nitrosylation). Cyclic GMP 193-197 nitric oxide synthase 3 Homo sapiens 34-67 18926858-10 2008 The results suggest that NO produced in smooth muscle cells as a result of the activation of eNOS by VIP exerts an autoinhibitory restraint on eNOS thereby regulating the balance of the VIP/cAMP/PKA and NO/cGMP/PKG pathways that regulate the relaxation of gut smooth muscle. Cyclic GMP 206-210 nitric oxide synthase 3 Homo sapiens 93-97 20360620-3 2010 Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP. Cyclic GMP 207-211 nitric oxide synthase 3 Homo sapiens 122-126 19176602-4 2009 Activity of NOS3 was characterized by conversion of arginine to citrulline, BH(4) intracellular availability, cGMP, and superoxide anion production. Cyclic GMP 110-114 nitric oxide synthase 3 Homo sapiens 12-16 19176602-7 2009 In aged cells with an uncoupled NOS3 as shown by the reduced BH(4) level, the increase in superoxide anion and the lower production of cGMP and the decrease in NO bioavailability were linearly correlated with the increase in basal [Ca(2+)](i). Cyclic GMP 135-139 nitric oxide synthase 3 Homo sapiens 32-36 18926858-10 2008 The results suggest that NO produced in smooth muscle cells as a result of the activation of eNOS by VIP exerts an autoinhibitory restraint on eNOS thereby regulating the balance of the VIP/cAMP/PKA and NO/cGMP/PKG pathways that regulate the relaxation of gut smooth muscle. Cyclic GMP 206-210 nitric oxide synthase 3 Homo sapiens 143-147 17974175-5 2007 There was applied a new method for treatment with mechanism of action stimulation the production cGMP of spermatozoa endothelial nitric oxide synthase (eNOS). Cyclic GMP 97-101 nitric oxide synthase 3 Homo sapiens 117-150 18641128-2 2008 We recently reported that endothelial nitric oxide synthase (eNOS)-derived NO regulates T cell receptor (TCR)-dependent ERK activation by a cGMP-independent mechanism. Cyclic GMP 140-144 nitric oxide synthase 3 Homo sapiens 26-59 18641128-2 2008 We recently reported that endothelial nitric oxide synthase (eNOS)-derived NO regulates T cell receptor (TCR)-dependent ERK activation by a cGMP-independent mechanism. Cyclic GMP 140-144 nitric oxide synthase 3 Homo sapiens 61-65 17502619-5 2007 Formation of this ternary complex among NOS-3, globular beta-actin, and Hsp90, in turn, results in an increase in both NOS activity and cyclic guanosine-3",5"-monophosphate, an index of bioactive NO, as well as an increased rate of Hsp90 degradation, thus limiting the duration for which NOS-3 remains activated. Cyclic GMP 136-172 nitric oxide synthase 3 Homo sapiens 40-45 17062240-7 2006 Gray unit values for cGMP, a downstream NO-signal-pathway molecule, showed results grossly corresponding to NOS-III activation. Cyclic GMP 21-25 nitric oxide synthase 3 Homo sapiens 108-115 17062240-9 2006 CONCLUSIONS: Significant activation of NOS-III and subsequent NO-cGMP signal pathway occurs in human cryopreserved allografts during the thawing process and can be significantly reduced by a NOS-III inhibitor administered during thawing. Cyclic GMP 65-69 nitric oxide synthase 3 Homo sapiens 191-198 16715118-10 2006 Activation of eNOS by myristoylated peptides was dependent on the PI3K/Akt pathway and the rise of intracellular calcium and was associated with an elevation of cGMP levels in PAEC and with relaxation of precontracted isolated pulmonary artery segments. Cyclic GMP 161-165 nitric oxide synthase 3 Homo sapiens 14-18 16725109-0 2006 VEGF-E activates endothelial nitric oxide synthase to induce angiogenesis via cGMP and PKG-independent pathways. Cyclic GMP 78-82 nitric oxide synthase 3 Homo sapiens 17-50 17040412-9 2006 Activation of the cGMP-pathway by sodium nitroprusside or its inhibition by guanylate cyclase (LY83583) or kinase (KT5823) inhibitors had more effects on fundus SMC, on which a higher expression of endothelial nitric oxide synthase was found. Cyclic GMP 18-22 nitric oxide synthase 3 Homo sapiens 198-231 15284089-7 2004 When HUVECs were subjected to a 0.5s impulse of 12 dynes/cm2, a transient disruption of the eNOS/PECAM-1 complex was observed, accompanied by an increase in eNOS activity (cGMP production). Cyclic GMP 172-176 nitric oxide synthase 3 Homo sapiens 92-96 16301818-12 2005 In addition, the beta3 adrenoceptor-dependent increase in cGMP and activation of NOS were blocked by the inhibition of phospholipase C (PLC), calcium/calmodulin (CaM), endothelial NOS activity and cGMP accumulation. Cyclic GMP 58-62 nitric oxide synthase 3 Homo sapiens 168-183 15284089-7 2004 When HUVECs were subjected to a 0.5s impulse of 12 dynes/cm2, a transient disruption of the eNOS/PECAM-1 complex was observed, accompanied by an increase in eNOS activity (cGMP production). Cyclic GMP 172-176 nitric oxide synthase 3 Homo sapiens 157-161 15288120-4 2004 Ionomycin induced citrulline and cGMP formation partially through phosphorylation of endothelial NO synthase (eNOS) at its serine residue 1177, which was mediated mainly by calmodulin-dependent kinase II. Cyclic GMP 33-37 nitric oxide synthase 3 Homo sapiens 110-114 14597568-9 2004 Activity of eNOS in HPMEC, measured over 48 h, either as the basal production of nitric oxide (NO) or as the accumulation of intracellular cGMP was not detectable. Cyclic GMP 139-143 nitric oxide synthase 3 Homo sapiens 12-16 14661033-3 2004 Exposure to hypoxia for 30 min led to a doubling in eNOS activity (control=6.2+/-4.4 vs hypoxia=14.1+/-5.0 fmol cGMP/microg protein, P<0.05) and NO release (control=5.9+/-0.8 vs hypoxia=11.8+/-1.2 nM/microg protein, P<0.05). Cyclic GMP 112-116 nitric oxide synthase 3 Homo sapiens 52-56 11668066-5 2001 Under basal conditions, the soluble mutant of eNOS appeared to be slightly more active than wild-type eNOS in terms of NO and cGMP formation, suggesting that membrane association may be crucial for inhibition of basal NO release but is not required for stimulation by Ca2+-mobilizing agents. Cyclic GMP 126-130 nitric oxide synthase 3 Homo sapiens 46-50 11668066-5 2001 Under basal conditions, the soluble mutant of eNOS appeared to be slightly more active than wild-type eNOS in terms of NO and cGMP formation, suggesting that membrane association may be crucial for inhibition of basal NO release but is not required for stimulation by Ca2+-mobilizing agents. Cyclic GMP 126-130 nitric oxide synthase 3 Homo sapiens 102-106 9409208-5 1997 cGMP production by AdeNOS-transduced cells was augmented by increasing intracellular levels of the eNOS cofactor tetrahydrobiopterin. Cyclic GMP 0-4 nitric oxide synthase 3 Homo sapiens 21-25 10601124-12 1999 NO serves as a negative-feedback regulator of eNOS expression via a cGMP-mediated process. Cyclic GMP 68-72 nitric oxide synthase 3 Homo sapiens 46-50 10440125-12 1999 CONCLUSION/INTERPRETATION: Human VSMC express cNOS, which is rapidly activated by insulin with a consequent increase of both cGMP and cAMP, suggesting that insulin-induced vasodilation in vivo is not entirely endothelium-mediated. Cyclic GMP 125-129 nitric oxide synthase 3 Homo sapiens 46-50 9518867-1 1998 UNLABELLED: Platelet cyclic guanosine monophosphate (cGMP) is produced by soluble guanylate cyclase (sGC), the activity of which is modulated by the activity of nitric oxide (NO) constitutive synthase (cNOS) which, in turn, is activated by a calcium/calmodulin complex. Cyclic GMP 21-51 nitric oxide synthase 3 Homo sapiens 202-206 9518867-1 1998 UNLABELLED: Platelet cyclic guanosine monophosphate (cGMP) is produced by soluble guanylate cyclase (sGC), the activity of which is modulated by the activity of nitric oxide (NO) constitutive synthase (cNOS) which, in turn, is activated by a calcium/calmodulin complex. Cyclic GMP 53-57 nitric oxide synthase 3 Homo sapiens 202-206 10974218-13 2000 cGMP levels were increased in eNOS-transduced compared to control cells. Cyclic GMP 0-4 nitric oxide synthase 3 Homo sapiens 30-34 10758392-7 2000 NOS-III activity was determined using TV-densitometry (gray units) and cGMP content using a semiquantitative score. Cyclic GMP 71-75 nitric oxide synthase 3 Homo sapiens 0-7 11112080-7 2000 Concentrations of cGMP were higher in eNOS-transduced lungs (13.2 +/- 2.3 vs 4.9 +/- 0.5 pmol/mg protein). Cyclic GMP 18-22 nitric oxide synthase 3 Homo sapiens 38-42 10329249-12 1999 Ca2+ is the principal activator of endothelial nitric oxide synthase (eNOS), which stimulates cyclic GMP production. Cyclic GMP 94-104 nitric oxide synthase 3 Homo sapiens 35-68 10329249-12 1999 Ca2+ is the principal activator of endothelial nitric oxide synthase (eNOS), which stimulates cyclic GMP production. Cyclic GMP 94-104 nitric oxide synthase 3 Homo sapiens 70-74 10329249-13 1999 The final result that the eNOS inhibitor L-NAME enhanced the histamine (100 microM) induced [Ca2+]i plateau suggests a negative feedback loop (via cGMP) of endothelial NO on its own synthesis in the regulation of endothelial [Ca2+]i signal. Cyclic GMP 147-151 nitric oxide synthase 3 Homo sapiens 26-30 8816908-8 1996 cNOS enzyme activity assessed by cGMP production in reporter cell fibroblasts was also lower in resistance arteries compared to conduit arteries (0.17 +/- 0.03 vs. 0.33 +/- 0.05 fmol cGMP/microgram protein, respectively; P < 0.05 resistance artery endothelium vs. conduit artery endothelium). Cyclic GMP 33-37 nitric oxide synthase 3 Homo sapiens 0-4 9314409-8 1997 Human eNOS gene delivery induces significant increases in urinary and aortic cGMP levels and urinary and serum nitrite/nitrate content (P<.05), while no significant differences in body weight, heart rate, water intake, food consumption, or urine excretion were observed. Cyclic GMP 77-81 nitric oxide synthase 3 Homo sapiens 6-10 9242548-6 1997 The eNOS transfectants were shown to contain functional enzyme by the conversion of L-arginine to L-citrulline in fractionated cells (P = .0001) and by exposing intact cells to calcium ionophore using the cGMP reporter cell assay (P = .0001). Cyclic GMP 205-209 nitric oxide synthase 3 Homo sapiens 4-8 8816908-8 1996 cNOS enzyme activity assessed by cGMP production in reporter cell fibroblasts was also lower in resistance arteries compared to conduit arteries (0.17 +/- 0.03 vs. 0.33 +/- 0.05 fmol cGMP/microgram protein, respectively; P < 0.05 resistance artery endothelium vs. conduit artery endothelium). Cyclic GMP 183-187 nitric oxide synthase 3 Homo sapiens 0-4 7882138-3 1994 In addition, this cGMP generation was abrogated in the presence of either a Ca2+ chelator, EGTA, or a calcium/calmodulin inhibitor, W7, suggesting that IL-4 stimulates the constitutive NOS (cNOS). Cyclic GMP 18-22 nitric oxide synthase 3 Homo sapiens 172-188 7583282-12 1995 These results support an astroglial location of the alpha 1-adrenoceptors and the cNOS that mediate NA stimulation of cGMP formation in cerebellum. Cyclic GMP 118-122 nitric oxide synthase 3 Homo sapiens 82-86 7882138-3 1994 In addition, this cGMP generation was abrogated in the presence of either a Ca2+ chelator, EGTA, or a calcium/calmodulin inhibitor, W7, suggesting that IL-4 stimulates the constitutive NOS (cNOS). Cyclic GMP 18-22 nitric oxide synthase 3 Homo sapiens 190-194 34638713-2 2021 In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP). Cyclic GMP 175-205 nitric oxide synthase 3 Homo sapiens 38-61 34635055-2 2021 There are multiple forms of cross-talk between the RhoA/ROCK pathway and the eNOS/NO/cGMP pathway, but previous work has not studied their interplay at a systems level. Cyclic GMP 85-89 nitric oxide synthase 3 Homo sapiens 77-81 34546460-8 2021 We also showed that the miR-182/Myadm relate BMP-TGF-beta pathway is associated with NOS3/NO/cGMP via the crosstalk between endothelial cells and smooth muscle cells. Cyclic GMP 93-97 nitric oxide synthase 3 Homo sapiens 85-89 34638713-2 2021 In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP). Cyclic GMP 175-205 nitric oxide synthase 3 Homo sapiens 63-67 34638713-2 2021 In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP). Cyclic GMP 207-211 nitric oxide synthase 3 Homo sapiens 38-61 34638713-2 2021 In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP). Cyclic GMP 207-211 nitric oxide synthase 3 Homo sapiens 63-67 33291075-4 2020 Mammalian target of rapamycin (mTOR) colocalized with PKG in pre-granulosa cells and was essential for eNOS/cGMP/PKG pathway-induced primordial follicle activation. Cyclic GMP 108-112 nitric oxide synthase 3 Homo sapiens 103-107 35466583-11 2022 CONCLUSION: Low androgen status up-regulated the expressions of patients in MAMs (FACL-4, PACS-2 and IP3R1) in the corpus cavernosum and inhibited the eNOS/NO/cGMP signaling pathway, resulting in impaired erectile function in rats. Cyclic GMP 159-163 nitric oxide synthase 3 Homo sapiens 151-155 33291075-5 2020 The eNOS/cGMP/PKG pathway was found to stabilize mTOR protein. Cyclic GMP 9-13 nitric oxide synthase 3 Homo sapiens 4-8 33291075-8 2020 However, agonists of the eNOS/cGMP/PKG pathway reduced FBXW7 mRNA levels. Cyclic GMP 30-34 nitric oxide synthase 3 Homo sapiens 25-29 33291075-9 2020 FBXW7 overexpression suppressed primordial follicle activation and prevented the eNOS/cGMP/PKG pathway from activating primordial follicles and stabilizing mTOR protein. Cyclic GMP 86-90 nitric oxide synthase 3 Homo sapiens 81-85 25913239-10 2015 Taken together, YLF-466D is capable of inhibiting platelet aggregation by activating AMPK and its downstream eNOS-cGMP-PKG signaling axis. Cyclic GMP 114-118 nitric oxide synthase 3 Homo sapiens 109-113 30367728-10 2019 The generation of NO and cGMP by diazoxide was blocked by an endothelial NOS (eNOS)-selective inhibitor, NIO, but not by a neuronal (n)NOS-selective inhibitor, Nomega -propyl-L-arginine (NPA). Cyclic GMP 25-29 nitric oxide synthase 3 Homo sapiens 61-76 32264405-5 2017 In the present study, we report that ZONF induce angiogenesis through MAPK/Akt/eNOS mediated nitric oxide formation, which further acts in a cGMP dependent manner. Cyclic GMP 141-145 nitric oxide synthase 3 Homo sapiens 79-83 27018249-0 2016 Tirofiban induces vasorelaxation of the coronary artery via an endothelium-dependent NO-cGMP signaling by activating the PI3K/Akt/eNOS pathway. Cyclic GMP 88-92 nitric oxide synthase 3 Homo sapiens 130-134 27018249-9 2016 These findings suggest that tirofiban induces vasorelaxation via an endothelium-dependent NO-cGMP signaling through the activation of the Akt/eNOS/sGC pathway. Cyclic GMP 93-97 nitric oxide synthase 3 Homo sapiens 142-146 32606304-5 2020 We found that beta-catenin depleted human umbilical vein ECs (HUVEC) stimulated with pharmacological activators of endothelial NO synthase (eNOS) showed a reduction in eNOS phosphorylation (Ser1177) as well as reduced intracellular cyclic guanosine monophosphate levels compared to control cells in static cultures. Cyclic GMP 232-262 nitric oxide synthase 3 Homo sapiens 115-138 32606304-5 2020 We found that beta-catenin depleted human umbilical vein ECs (HUVEC) stimulated with pharmacological activators of endothelial NO synthase (eNOS) showed a reduction in eNOS phosphorylation (Ser1177) as well as reduced intracellular cyclic guanosine monophosphate levels compared to control cells in static cultures. Cyclic GMP 232-262 nitric oxide synthase 3 Homo sapiens 140-144 31547684-0 2019 Botulinum toxin type A suppresses arterial vasoconstriction by regulating calcium sensitization and the endothelium-dependent endothelial nitric oxide synthase/soluble guanylyl cyclase/cyclic guanosine monophosphate pathway: An in vitro study. Cyclic GMP 185-215 nitric oxide synthase 3 Homo sapiens 126-159 26655728-2 2016 Nitric oxide (NO) generated by vascular endothelial NO synthase (eNOS) plays a critical role in the NO/ cyclic guanosine 5"-monophosphate (cGMP)-mediated pulmonary vascular function. Cyclic GMP 139-143 nitric oxide synthase 3 Homo sapiens 65-69 26655728-3 2016 Here we examined whether internalization of a fifteen amino acid (KRFNSISCSSWRRKR) synthetic peptide (P3) enhances the catalytic activity of eNOS via caveolae/eNOS dissociation leading to NO release and increased cGMP production in pulmonary artery endothelial cells (EC). Cyclic GMP 213-217 nitric oxide synthase 3 Homo sapiens 141-145 26351364-7 2015 A guanosine 3",5"-cyclic monophosphate (cGMP) antagonist reversed KMUP-1-induced ROCK II reduction, indicating cGMP/eNOS involvement. Cyclic GMP 2-38 nitric oxide synthase 3 Homo sapiens 116-120 26351364-7 2015 A guanosine 3",5"-cyclic monophosphate (cGMP) antagonist reversed KMUP-1-induced ROCK II reduction, indicating cGMP/eNOS involvement. Cyclic GMP 40-44 nitric oxide synthase 3 Homo sapiens 116-120 24827148-5 2014 Furthermore, pretreatment with a p38 mitogen-activated protein kinase (p38 MAPK) inhibitor suppressed the increased phosphorylation level of eNOS and intracellular cGMP concentration. Cyclic GMP 164-168 nitric oxide synthase 3 Homo sapiens 141-145 25733135-4 2015 In this review, we aim to place the genomic findings on components of the NO/cGMP pathway, namely endothelial nitric oxide synthase, soluble guanylyl cyclase and phosphodiesterase 5A, in context of preventive and therapeutic strategies for treating atherosclerosis and its sequelae. Cyclic GMP 77-81 nitric oxide synthase 3 Homo sapiens 98-131 24909615-10 2014 In contrast to iNOS, endothelial NOS-driven cGMP-dependent signaling promoted mitochondrial function and survival of MG132-stressed cells. Cyclic GMP 44-48 nitric oxide synthase 3 Homo sapiens 21-36 24914683-6 2014 Incubation with exogenous NO, a GC activator, or a cGMP analog reversed the effect of eNOS knockdown, while the effect of NO was blocked by inhibition of GC. Cyclic GMP 51-55 nitric oxide synthase 3 Homo sapiens 86-90 24914683-11 2014 These effects were reversed by adenosine, an effect mediated by eNOS-synthesized NO, acting via soluble guanylate cyclase/cGMP to activate a mitochondrial biogenesis regulatory program under the control of PGC-1alpha. Cyclic GMP 122-126 nitric oxide synthase 3 Homo sapiens 64-68 24379783-2 2013 In blood vessels, it is synthesized in a dynamic fashion by endothelial nitric oxide synthase (eNOS) and influences vascular function via two distinct mechanisms, the activation of soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)-dependent signaling and the S-nitrosylation of proteins with reactive thiols (S-nitrosylation). Cyclic GMP 212-242 nitric oxide synthase 3 Homo sapiens 60-93 24138560-8 2014 CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis. Cyclic GMP 163-193 nitric oxide synthase 3 Homo sapiens 115-148 24379783-2 2013 In blood vessels, it is synthesized in a dynamic fashion by endothelial nitric oxide synthase (eNOS) and influences vascular function via two distinct mechanisms, the activation of soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)-dependent signaling and the S-nitrosylation of proteins with reactive thiols (S-nitrosylation). Cyclic GMP 212-242 nitric oxide synthase 3 Homo sapiens 95-99 24379783-2 2013 In blood vessels, it is synthesized in a dynamic fashion by endothelial nitric oxide synthase (eNOS) and influences vascular function via two distinct mechanisms, the activation of soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)-dependent signaling and the S-nitrosylation of proteins with reactive thiols (S-nitrosylation). Cyclic GMP 244-248 nitric oxide synthase 3 Homo sapiens 95-99 22517552-10 2012 This effect is mediated by the activation of the PKCdelta/eNOS/NO/cGMP pathway. Cyclic GMP 66-70 nitric oxide synthase 3 Homo sapiens 58-62 23341020-12 2013 Endothelial nitric oxide synthase (eNOS) phosphorylation via the cAMP/PKA and AMPK pathways and consequent activation of the soluble guanylyl cyclase/cyclic guanosine monophosphate pathway might play an important role in cilostazol-induced vasodilation of the retinal arterioles. Cyclic GMP 150-180 nitric oxide synthase 3 Homo sapiens 0-33 22716077-1 2012 In a brief overview, in NO-sGC-cGMP signaling in a blood vessel, l-arginine is converted in the endothelium monolayer by the endothelial nitric oxide synthase (eNOS) to NO which diffuses into both the vessel lumen and the vessel wall, thereby activating soluble guanylate cyclase (sGC). Cyclic GMP 31-35 nitric oxide synthase 3 Homo sapiens 125-158