PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30318767-11 2019 Moreover, in the LPS group, the sGC inhibitor ODQ, the PKG inhibitor Rp-8-Br and the PKC inhibitor GF109203X abrogated the increased p47phox phosphorylation and reduced the ROS levels. Reactive Oxygen Species 173-176 protein kinase cGMP-dependent 1 Homo sapiens 55-58 30318767-12 2019 In conclusion, selective inhibitors of cGMP-PKG and PKC-p47phox pathways that regulate ROS generation by LPS in platelets may help control the redox balance in sepsis improving the survival of patients. Reactive Oxygen Species 87-90 protein kinase cGMP-dependent 1 Homo sapiens 44-47 24277866-10 2014 Taken together, these findings suggest that NO modulates ventricular sarcK(ATP) channels via a novel sGC-cGMP-PKG-ROS(H2O2)-ERK1/2-calmodulin-CaMKII (delta isoform in particular) signalling cascade, which heightens K(ATP) channel activity by destabilizing the long closed states while facilitating closed-to-open state transitions. Reactive Oxygen Species 114-117 protein kinase cGMP-dependent 1 Homo sapiens 110-113 29962348-3 2018 Reactive Oxygen Species (ROS) can activate protein kinases: CaMKII, PKG, PKA, ERK, PI3K, Akt, PKC, PDK, JNK, p38. Reactive Oxygen Species 0-23 protein kinase cGMP-dependent 1 Homo sapiens 68-71 29962348-3 2018 Reactive Oxygen Species (ROS) can activate protein kinases: CaMKII, PKG, PKA, ERK, PI3K, Akt, PKC, PDK, JNK, p38. Reactive Oxygen Species 25-28 protein kinase cGMP-dependent 1 Homo sapiens 68-71 25762630-3 2015 This synergistic effect requires the generation of reactive oxygen species (ROS) from H89 and NO from GTN treatment that causes cGMP production and PKG activation. Reactive Oxygen Species 51-74 protein kinase cGMP-dependent 1 Homo sapiens 148-151 25762630-3 2015 This synergistic effect requires the generation of reactive oxygen species (ROS) from H89 and NO from GTN treatment that causes cGMP production and PKG activation. Reactive Oxygen Species 76-79 protein kinase cGMP-dependent 1 Homo sapiens 148-151 25904916-0 2015 KCa3.1/IK1 Channel Regulation by cGMP-Dependent Protein Kinase (PKG) via Reactive Oxygen Species and CaMKII in Microglia: An Immune Modulating Feedback System? Reactive Oxygen Species 73-96 protein kinase cGMP-dependent 1 Homo sapiens 64-67 25904916-6 2015 The same site is potentially phosphorylated by cGMP kinase (PKG), and in some cells, PKG can increase Ca(2+), CaM activation, and ROS. Reactive Oxygen Species 130-133 protein kinase cGMP-dependent 1 Homo sapiens 60-63 25904916-6 2015 The same site is potentially phosphorylated by cGMP kinase (PKG), and in some cells, PKG can increase Ca(2+), CaM activation, and ROS. Reactive Oxygen Species 130-133 protein kinase cGMP-dependent 1 Homo sapiens 85-88 25904916-8 2015 Elevating cGMP increased both the KCa3.1 current and intracellular ROS production, and both were prevented by the selective PKG inhibitor, KT5823. Reactive Oxygen Species 67-70 protein kinase cGMP-dependent 1 Homo sapiens 124-127 25904916-9 2015 The cGMP/PKG-evoked increase in KCa3.1 current in intact MLS-9 microglia was mediated by ROS, mimicked by applying hydrogen peroxide (H2O2), inhibited by a ROS scavenger (MGP), and prevented by a selective CaMKII inhibitor (mAIP). Reactive Oxygen Species 89-92 protein kinase cGMP-dependent 1 Homo sapiens 9-12 25904916-9 2015 The cGMP/PKG-evoked increase in KCa3.1 current in intact MLS-9 microglia was mediated by ROS, mimicked by applying hydrogen peroxide (H2O2), inhibited by a ROS scavenger (MGP), and prevented by a selective CaMKII inhibitor (mAIP). Reactive Oxygen Species 156-159 protein kinase cGMP-dependent 1 Homo sapiens 9-12 25385631-5 2014 The mechanism of protection appears to be triggered by reactive oxygen species (ROS) and involves known IPC signaling components such as PKG and PKC epsilon in addition to the mitochondrial ATP-sensitive K(+) channel. Reactive Oxygen Species 55-78 protein kinase cGMP-dependent 1 Homo sapiens 137-140 25385631-5 2014 The mechanism of protection appears to be triggered by reactive oxygen species (ROS) and involves known IPC signaling components such as PKG and PKC epsilon in addition to the mitochondrial ATP-sensitive K(+) channel. Reactive Oxygen Species 80-83 protein kinase cGMP-dependent 1 Homo sapiens 137-140 20547753-8 2010 These results show that NO-mediated downregulation of PGC-1 alpha is necessary for NO-induced endothelial migration and that NO/protein kinase G (PKG)-dependent downregulation of PGC-1 alpha and the ROS detoxification system in endothelial cells are mediated by the PI3K/Akt signaling pathway and subsequent inactivation of the FoxO transcription factor Foxo3a. Reactive Oxygen Species 199-202 protein kinase cGMP-dependent 1 Homo sapiens 125-144 21672583-9 2011 Moreover, SNP-induced increase in intracellular Ca(2+) levels, ROS production and decrease in cell viability were blocked by a cGMP-dependent protein kinase (PKG) inhibitor. Reactive Oxygen Species 63-66 protein kinase cGMP-dependent 1 Homo sapiens 158-161 20547753-8 2010 These results show that NO-mediated downregulation of PGC-1 alpha is necessary for NO-induced endothelial migration and that NO/protein kinase G (PKG)-dependent downregulation of PGC-1 alpha and the ROS detoxification system in endothelial cells are mediated by the PI3K/Akt signaling pathway and subsequent inactivation of the FoxO transcription factor Foxo3a. Reactive Oxygen Species 199-202 protein kinase cGMP-dependent 1 Homo sapiens 146-149 18006449-4 2008 PKG phosphorylates a protein on the mitochondrial outer membrane (MOM), which then causes the mitochondrial K(ATP) channel (mitoK(ATP)) on the mitochondrial inner membrane to open, leading to increased production of reactive oxygen species (ROS) by the mitochondria. Reactive Oxygen Species 216-239 protein kinase cGMP-dependent 1 Homo sapiens 0-3 20053925-8 2010 Altogether, in this report we provide novel evidence that activation of PKG stimulates neuronal K(ATP) channels by modulating intrinsic channel gating via a 5-HD-sensitive factor(s)/ROS/Ca(2+)/calmodulin signaling pathway that requires the presence of the SUR1 subunit. Reactive Oxygen Species 182-185 protein kinase cGMP-dependent 1 Homo sapiens 72-75 18037907-9 2008 CONCLUSIONS AND IMPLICATIONS: Nitrate tolerance induced by NTG at low concentrations may result from an increased production of reactive oxygen species acting on sites upstream of PKG. Reactive Oxygen Species 128-151 protein kinase cGMP-dependent 1 Homo sapiens 180-183 18006449-4 2008 PKG phosphorylates a protein on the mitochondrial outer membrane (MOM), which then causes the mitochondrial K(ATP) channel (mitoK(ATP)) on the mitochondrial inner membrane to open, leading to increased production of reactive oxygen species (ROS) by the mitochondria. Reactive Oxygen Species 241-244 protein kinase cGMP-dependent 1 Homo sapiens 0-3 16037573-2 2005 Activated PKG opens mitochondrial KATP channels (mitoKATP) which increase production of reactive oxygen species. Reactive Oxygen Species 88-111 protein kinase cGMP-dependent 1 Homo sapiens 10-13 14656708-7 2004 KT-5823, an inhibitor of PKG, prevented ROS generation, indicating that PKG is required for ROS generation. Reactive Oxygen Species 40-43 protein kinase cGMP-dependent 1 Homo sapiens 72-75 14656708-7 2004 KT-5823, an inhibitor of PKG, prevented ROS generation, indicating that PKG is required for ROS generation. Reactive Oxygen Species 92-95 protein kinase cGMP-dependent 1 Homo sapiens 72-75 14656708-8 2004 In addition, 8-bromoguanosine 3",5"-cyclic monophosphate (8-BrcGMP), an activator of PKG, induced ROS generation. Reactive Oxygen Species 98-101 protein kinase cGMP-dependent 1 Homo sapiens 85-88 14656708-16 2004 These results suggest that SNAP-induced ROS generation is mediated by activation of PKG and mitochondrial K(ATP) channels and that opening of mitochondrial K(ATP) channels is the downstream event of PKG activation. Reactive Oxygen Species 40-43 protein kinase cGMP-dependent 1 Homo sapiens 84-87 14656708-0 2004 Exogenous nitric oxide generates ROS and induces cardioprotection: involvement of PKG, mitochondrial KATP channels, and ERK. Reactive Oxygen Species 33-36 protein kinase cGMP-dependent 1 Homo sapiens 82-85 14656708-1 2004 We examined whether cGMP-dependent protein kinase (PKG) and mitochondrial ATP-sensitive potassium (K(ATP)) channels are involved in S-nitroso-N-acetyl penicillamine (SNAP)-induced reactive oxygen species (ROS) generation. Reactive Oxygen Species 180-203 protein kinase cGMP-dependent 1 Homo sapiens 51-54 14656708-7 2004 KT-5823, an inhibitor of PKG, prevented ROS generation, indicating that PKG is required for ROS generation. Reactive Oxygen Species 40-43 protein kinase cGMP-dependent 1 Homo sapiens 25-28