PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32268802-0 2020 Hydrogen sulfide attenuates diabetic neuropathic pain through NO/cGMP/PKG pathway and mu-opioid receptor. Hydrogen Sulfide 0-16 protein kinase cGMP-dependent 1 Homo sapiens 70-73 25444755-5 2015 Mechanistically, PDE5 inhibitors protect the heart against I/R injury through increased expression of nitric oxide synthases, activation of protein kinase G (PKG), PKG-dependent hydrogen sulfide generation, and phosphorylation of glycogen synthase kinase-3beta - a master switch immediately proximal to mitochondrial permeability transition pore and the end effector of cardioprotection. Hydrogen Sulfide 178-194 protein kinase cGMP-dependent 1 Homo sapiens 164-167 28705807-0 2017 Augmentation of cGMP/PKG pathway and colonic motility by hydrogen sulfide. Hydrogen Sulfide 57-73 protein kinase cGMP-dependent 1 Homo sapiens 21-24 28705807-5 2017 H2S levels were increased in response to l-cysteine, and the effect of l-cysteine was augmented by GSNO in a cGMP-dependent protein kinase-sensitive manner, suggesting augmentation of CSE/H2S by cGMP/PKG pathway. Hydrogen Sulfide 0-3 protein kinase cGMP-dependent 1 Homo sapiens 200-203 28705807-9 2017 NO generates H2S via cGMP/PKG pathway, and H2S, in turn, inhibits PDE5 activity and augments NO-induced cGMP levels. Hydrogen Sulfide 13-16 protein kinase cGMP-dependent 1 Homo sapiens 26-29 28705807-12 2017 H2S inhibits phosphodiesterase 5 activity to augment cGMP levels in response to NO, which, in turn, via cGMP/PKG pathway, generates H2S. Hydrogen Sulfide 0-3 protein kinase cGMP-dependent 1 Homo sapiens 109-112 28705807-12 2017 H2S inhibits phosphodiesterase 5 activity to augment cGMP levels in response to NO, which, in turn, via cGMP/PKG pathway, generates H2S. Hydrogen Sulfide 132-135 protein kinase cGMP-dependent 1 Homo sapiens 109-112 29470646-9 2018 CO inhibits H2S production through inactivation of CSE by PKG-dependent phosphorylation. Hydrogen Sulfide 12-15 protein kinase cGMP-dependent 1 Homo sapiens 58-61 27784679-9 2017 Finally, H2S-derived polysulfides directly activate cGMP-dependent protein kinase (PKG). Hydrogen Sulfide 9-12 protein kinase cGMP-dependent 1 Homo sapiens 83-86 27509878-0 2016 Urothelium muscarinic activation phosphorylates CBS(Ser227) via cGMP/PKG pathway causing human bladder relaxation through H2S production. Hydrogen Sulfide 122-125 protein kinase cGMP-dependent 1 Homo sapiens 69-72 27509878-9 2016 The increase in H2S production and in turn of cGMP is driven by CBS-cGMP/PKG-dependent phosphorylation at Ser(227) following carbachol stimulation. Hydrogen Sulfide 16-19 protein kinase cGMP-dependent 1 Homo sapiens 73-76 27509878-10 2016 The finding of the presence of this crosstalk between the cGMP/PKG and H2S pathway downstream to the M1/M3 receptor in the human urothelium further implies a key role for H2S in bladder physiopathology. Hydrogen Sulfide 171-174 protein kinase cGMP-dependent 1 Homo sapiens 63-66 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. Hydrogen Sulfide 29-32 protein kinase cGMP-dependent 1 Homo sapiens 194-197 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. Hydrogen Sulfide 83-86 protein kinase cGMP-dependent 1 Homo sapiens 194-197 22570497-4 2012 Exposure of endothelial cells to H(2)S increases intracellular cyclic guanosine 5"-monophosphate (cGMP) in a NO-dependent manner, and activated protein kinase G (PKG) and its downstream effector, the vasodilator-stimulated phosphoprotein (VASP). Hydrogen Sulfide 33-38 protein kinase cGMP-dependent 1 Homo sapiens 144-160 22570497-5 2012 Inhibition of endothelial isoform of NO synthase (eNOS) or PKG-I abolishes the H(2)S-stimulated angiogenic response, and attenuated H(2)S-stimulated vasorelaxation, demonstrating the requirement of NO in vascular H(2)S signaling. Hydrogen Sulfide 79-84 protein kinase cGMP-dependent 1 Homo sapiens 59-62 22570497-4 2012 Exposure of endothelial cells to H(2)S increases intracellular cyclic guanosine 5"-monophosphate (cGMP) in a NO-dependent manner, and activated protein kinase G (PKG) and its downstream effector, the vasodilator-stimulated phosphoprotein (VASP). Hydrogen Sulfide 33-38 protein kinase cGMP-dependent 1 Homo sapiens 162-165 23285278-9 2012 Treatment of aortic rings with NaHS, a fast releasing H2S donor, enhanced phosphorylation of vasodilator-stimulated phosphoprotein in a time-dependent manner, suggesting that cGMP-dependent protein kinase (PKG) is activated after exposure to H2S. Hydrogen Sulfide 242-245 protein kinase cGMP-dependent 1 Homo sapiens 206-209 23285278-12 2012 Dilatory responses to NaHS and L-cysteine (a substrate for H2S production) were reduced in vessels of PKG-I knockout mice (PKG-I-/-). Hydrogen Sulfide 59-62 protein kinase cGMP-dependent 1 Homo sapiens 102-105 23285278-12 2012 Dilatory responses to NaHS and L-cysteine (a substrate for H2S production) were reduced in vessels of PKG-I knockout mice (PKG-I-/-). Hydrogen Sulfide 59-62 protein kinase cGMP-dependent 1 Homo sapiens 123-126