PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11331261-11 2001 CONCLUSIONS: We therefore conclude that increased expression of sGC in the setting of tolerance reflects a chronic inhibition rather than an induction of the sGC-cGK-I pathway and may be mediated at least in part by increased vascular superoxide. Superoxides 235-245 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 64-67 9051308-18 1997 Basal and YC-1-stimulated sGC activity was sensitive to inhibition by superoxide (O-2) generated by xanthine/xanthine oxidase, and was protected from this inhibition by superoxide dismutase (SOD). Superoxides 70-80 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 26-29 9452441-1 1998 Nitric oxide (NO), a physiologically important activator of soluble guanylyl cyclase (sGC), is synthesized from L-arginine and O2 in a reaction catalyzed by NO synthases (NOS). Superoxides 127-129 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 86-89 9708036-10 1998 Our results provide the first evidence that excess superoxide production in hypertension may trigger a desensitization of vascular sGC. Superoxides 51-61 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 131-134 9051308-18 1997 Basal and YC-1-stimulated sGC activity was sensitive to inhibition by superoxide (O-2) generated by xanthine/xanthine oxidase, and was protected from this inhibition by superoxide dismutase (SOD). Superoxides 82-85 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 26-29 17196179-12 2007 Thus, the study documented regional distributions of NOS, NAD(P)H oxidase, antioxidant enzymes, sGC and calmodulin which collectively regulate production and biological activities of NO and superoxide, the two important small molecular size signaling molecules. Superoxides 190-200 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 96-99 24907870-6 2014 NO/heme-independent sGC activation provided protection over ACE inhibition against mitochondrial superoxide production and progressive fibrotic remodeling, ultimately leading to a further improvement of cardiac performance, hypertrophic growth and heart failure. Superoxides 97-107 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 20-23 20522591-7 2010 Chronic treatment with the sGC activator HMR1766 improved NO sensitivity and endothelial function, reduced CYP2E1 expression and superoxide formation, enhanced 20-HETE levels, and reversed the contractile deficit observed in the diabetic rats that received placebo. Superoxides 129-139 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 27-30 25329747-0 2015 Different influences of extracellular and intracellular superoxide on relaxation through the NO/sGC/cGMP pathway in isolated rat iliac arteries. Superoxides 56-66 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 93-99 25329747-1 2015 Superoxide production is increased in diseased blood vessels, which is considered to lead to impairment of the nitric oxide (NO)/soluble guanylate cyclase (sGC)/cGMP pathway. Superoxides 0-10 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 156-159 25329747-10 2015 These findings suggest that extracellular superoxide reacts with NO only outside the cell, whereas intracellular superoxide not only scavenges NO inside the cell but also shifts the sGC redox equilibrium. Superoxides 42-52 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 182-185 25329747-10 2015 These findings suggest that extracellular superoxide reacts with NO only outside the cell, whereas intracellular superoxide not only scavenges NO inside the cell but also shifts the sGC redox equilibrium. Superoxides 113-123 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 182-185 12676772-8 2003 These complexes likely function to stabilize sGC as well as to provide directed intracellular transfer of NO from NOS to sGC, thus preventing inactivation of NO by superoxide anion and formation of peroxynitrite, which is a toxic molecule that has been implicated in the pathology of several vascular diseases. Superoxides 164-180 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 45-48 12676772-8 2003 These complexes likely function to stabilize sGC as well as to provide directed intracellular transfer of NO from NOS to sGC, thus preventing inactivation of NO by superoxide anion and formation of peroxynitrite, which is a toxic molecule that has been implicated in the pathology of several vascular diseases. Superoxides 164-180 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 121-124 13678534-8 2003 When STZ-treated animals were posttreated with a derivative of superoxide dismutase that stays in circulation without undergoing renal ultrafiltration, immunoreactivities to MoAb3221 but not to MoAb28131 increased markedly in diabetic retina, suggesting that superoxide cancels free NO for local sGC activation. Superoxides 63-73 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 296-299 13678534-9 2003 These results provide evidence of aberrant utilization of NO and suggest that superoxide plays a role in interfering with NO-mediated sGC activation for phototransducing events in this neural tissue. Superoxides 78-88 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 134-137 15312990-4 2004 We aimed to investigate whether superoxide and peroxynitrite impacts on the expression and function of sGC and if such a mechanism occurs in a hypercholestemia-induced atherosclerosis. Superoxides 32-42 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 103-106 15312990-6 2004 Furthermore, intracellular superoxide as generated by LY85385 almost completely inhibited sGC-activity and increased its expression. Superoxides 27-37 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 90-93