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1 I)PPIX remains four coordinate when bound to soluble guanylyl cyclase.
2 Four-coordinate metalloporphyrins activate soluble guanylyl cyclase.
3 old rats do not express the beta subunit of soluble guanylyl cyclase.
4 receptors act by NO-mediated stimulation of soluble guanylyl cyclase.
5 ex, which, among other functions, stabilizes soluble guanylyl cyclase.
6 endothelial nitric oxide synthase (NOS) and soluble guanylyl cyclase.
7 quires endothelial nitric oxide synthase and soluble guanylyl cyclase.
8 d suppression of NF-kappaB and activation of soluble guanylyl cyclase.
9 ERK pathway and the subsequent activation of soluble guanylyl cyclase.
10 is via endothelial nitric-oxide synthase and soluble guanylyl cyclase.
11 by maintaining the synaptic localization of soluble guanylyl cyclase.
12 smaller extent, by the direct stimulation of soluble guanylyl cyclase.
13 show similarity to the regulatory domain of soluble guanylyl cyclases.
15 nor was partially blocked by an inhibitor of soluble guanylyl cyclase, 1H-[1,2,4]oxadiazolo[4,3, -a]q
17 2 receptors to stimulate cGMP production via soluble guanylyl cyclase activation and absorption throu
18 vailability of NO would be too low to elicit soluble guanylyl cyclase activation in the presence of b
19 play an important role in NO generation and soluble guanylyl cyclase activation under hypoxic condit
22 measured in distal human PASMCs treated with soluble guanylyl cyclase activators (nitric oxide donors
23 and cAMP-dependent mechanism for modulating soluble guanylyl cyclase activity in pituitary cells.
25 (S-nitroso-N-acetyl-DL-penicillamine) and a soluble guanylyl cyclase agonist (YC-1) mimicked AMPA ef
28 3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, also blocked the effects of ni
33 The stimulatory role of NOS is mediated by soluble guanylyl cyclase and results from a cGMP-depende
35 of Dictyostelium discoideum, a heterodimeric soluble guanylyl cyclase, and a homodimeric membrane gua
36 te transporters, nitric oxide (NO) synthase, soluble guanylyl cyclase, and ATP-sensitive potassium (K
37 esent study, we determined the role of cGMP, soluble guanylyl cyclase, and protein kinase G in the po
38 and by sodium nitroprusside, an activator of soluble guanylyl cyclase, and was potentiated by a cGMP-
39 ts is due to the lack of the beta subunit of soluble guanylyl cyclase, and we speculate that this def
41 ups in both Ni(II)- and Cu(II)-reconstituted soluble guanylyl cyclase are consistent with a substanti
43 The mechanism was due to the activation of soluble guanylyl cyclase because 8-bromo-cyclic GMP acti
44 ffects of CO in this study were mediated via soluble guanylyl cyclase, because 1H-(1,2,4)oxadiazole (
46 by N(G)-nitro-L-arginine methyl ester and of soluble guanylyl cyclase by 1H-[1,2,4]oxadiazolo[4,3,-a]
47 d receptors stimulate nitric oxide-sensitive soluble guanylyl cyclase by increasing intracellular Ca(
49 tro-L-arginine methyl ester) and blockade of soluble guanylyl cyclase (by ODQ; 1H-1,2,4-oxadiazolo[4,
50 MP analog 8-bromo-cGMP, as well as by the NO-soluble guanylyl cyclase-cGMP signaling inhibitor thromb
51 ulator BAY-41-2272 converts the CO adduct of soluble guanylyl cyclase (CO-sGC) enzyme from a low- to
52 ese data support a model where activation of soluble guanylyl cyclase correlates with the absence of
53 nisms through which NO generally acts is the soluble guanylyl cyclase-cyclic GMP (sGC-cGMP) pathway.
54 d protein modification, biologically through soluble guanylyl-cyclase-dependent modulation of the MMP
55 , we have identified a link between impaired soluble-guanylyl-cyclase-dependent nitric oxide signalli
57 .By blocking the activity of NO synthase and soluble guanylyl cyclase enzymes after training, we prov
60 ht to be mediated by the action of NO on the soluble guanylyl cyclase (GC) in the smooth muscle and s
62 ric oxide synthase (NOS) and the NO receptor-soluble guanylyl cyclase (GC), the activation of which l
64 iven pRb hyperphosphorylation occurs through soluble guanylyl cyclase/guanosine 3',5'-cyclic monophos
66 contains three genes that code for atypical soluble guanylyl cyclases: Gyc-88E, Gyc-89Da, and Gyc-89
70 uanylyl cyclases and of 7 gcy genes encoding soluble guanylyl cyclases in the complete genome sequenc
71 imulated fluid absorption was blocked by the soluble guanylyl cyclase inhibitor 1-H-[1,2,4]oxadiazolo
72 n viable cells, which was not blocked by the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[
73 romo-cyclic GMP activated PI3 kinase and the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[
74 this lusitropic effect was attenuated by the soluble guanylyl cyclase inhibitor 1H:-[1,2,4]oxadiazolo
76 ,4)oxadiazole (4,3-alpha) quinoxaline-1-one (soluble guanylyl cyclase inhibitor) completely reversed
77 e to anoxic conditions and is blocked by the soluble guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo
78 These effects were inhibited by LY 83583, a soluble guanylyl cyclase inhibitor, and mimicked by 8-Br
82 ,2,4]-oxadiazolo-[4,3-a]quinoxalin-1-one) (a soluble guanylyl cyclase-inhibitor, Rp-8-(4-chlorophenyl
83 he presence of various phosphodiesterase and soluble guanylyl cyclase inhibitors, confirming that G(s
85 GMP; though H(2)S does not directly activate soluble guanylyl cyclase, it maintains a tonic inhibitor
87 by the additional presence of inhibitors of soluble guanylyl cyclase (LY83583) or protein kinase G (
88 xpression of Foxp3 in MBP-primed T cells via soluble guanylyl cyclase-mediated production of cGMP.
89 icroM 8-Bromo-cGMP), and (iii) inhibition of soluble guanylyl cyclase (ODQ (1H-[1,2,4,]oxadiazolo(4,3
92 agents that release nitric oxide, stimulate soluble guanylyl cyclase, or activate cGMP-dependent pro
93 e conclude that NO production, activation of soluble guanylyl cyclase, or changes in intracellular cG
95 rom digenic mutation carriers contained less soluble guanylyl cyclase protein and consequently displa
97 e synthase (eNOS) by directly activating its soluble guanylyl cyclase receptor, rescued blood vessel
98 n-1-one, inhibitors of NO synthase (NOS) and soluble guanylyl cyclase, respectively, abolished tadala
99 sine 3',5'-cyclic monophosphate ([cGMP]i) by soluble guanylyl cyclase, resulting in fast onset and lo
100 , we demonstrate the effect of NO donors and soluble guanylyl cyclase (sGC) activators in differentia
103 y firmly established endogenous modulator of soluble guanylyl cyclase (sGC) activity, but physiologic
105 e isoforms (ACs 1-9), a structurally related soluble guanylyl cyclase (sGC) and a soluble AC (sAC).
107 indicates that the functional properties of soluble guanylyl cyclase (sGC) are affected not only by
108 e have identified the alpha1-subunit gene of soluble guanylyl cyclase (sGC) as a novel androgen-regul
109 Heme insertion is key during maturation of soluble guanylyl cyclase (sGC) because it enables sGC to
110 of recombinant nitric oxide (NO)-stimulated soluble guanylyl cyclase (SGC) by Ca2+ was demonstrated.
111 r diseases with the oxidation of the heme of soluble guanylyl cyclase (sGC) critically implicated in
113 nce that treatment with NO donors stimulates soluble guanylyl cyclase (sGC) in the MCC, and as a resu
114 9A mRNA expression closely resembles that of soluble guanylyl cyclase (sGC) in the rat brain, suggest
115 l-L-arginine (NMMA); 300 or 500 microM) or a soluble guanylyl cyclase (sGC) inhibitor (1H-[1,2,4]oxad
116 ase in cell volume that was abolished by the soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadi
117 -nitro-L-arginine methyl ester; 30 mg/kg), a soluble guanylyl cyclase (sGC) inhibitor [1H-(1, 2, 4) o
118 nt with either a nitric oxide scavenger or a soluble guanylyl cyclase (sGC) inhibitor diminished the
126 e of nitric oxide (NO) in the stimulation of soluble guanylyl cyclase (sGC) is well established, but
127 ts of cGMP levels in this pathway, including soluble guanylyl cyclase (sGC) itself, the NO -activated
128 of cAMP and cGMP in the above effects using soluble guanylyl cyclase (sGC) or adenylate cyclase (AC)
129 have shown that the levels of expression of soluble guanylyl cyclase (sGC) or cGMP-dependent protein
131 blots for endothelial NO synthase (eNOS) and soluble guanylyl cyclase (sGC) revealed reduced eNOS exp
134 cular and neuronal systems via activation of soluble guanylyl cyclase (sGC), a heme-containing hetero
135 s in the brain largely through activation of soluble guanylyl cyclase (sGC), a heterodimer comprised
136 s in the brain largely through activation of soluble guanylyl cyclase (sGC), a heterodimer comprising
137 1A3, which encodes the alpha1 subunit of the soluble guanylyl cyclase (sGC), a key enzyme in the nitr
140 proximately 9% contained the beta subunit of soluble guanylyl cyclase (sGC), a major target of NO.
141 of neuronal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC), and can be mimicked by t
143 tion of the major downstream effector of NO, soluble guanylyl cyclase (sGC), in the superficial dorsa
146 by localizing the expression and activity of soluble guanylyl cyclase (SGC), its principal molecular
147 ignaling through activation of its receptor, soluble guanylyl cyclase (sGC), leading to elevation of
149 ,3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase (sGC), or Rp-8-Br-cGMP, an inhi
150 in the presence of inhibitors selective for soluble guanylyl cyclase (sGC), PKG, calmodulin, CaMKII
151 ted optic nerve, nitric oxide (NO) activates soluble guanylyl cyclase (sGC), resulting in a selective
152 h structural homology to the beta subunit of soluble guanylyl cyclase (sGC), suggesting a NO sensing
153 n yet is homologous to the central region in soluble guanylyl cyclase (sGC), the main receptor for ni
154 he molecular mechanism of desensitization of soluble guanylyl cyclase (sGC), the NO receptor, has lon
157 clinically vasoactive through stimulation of soluble guanylyl cyclase (sGC), which produces the secon
158 onducted to determine whether NO activates a soluble guanylyl cyclase (sGC)-cyclic guanosine monophos
167 s that investigated the regulation of the NO/soluble guanylyl cyclase (sGC)/cGMP pathway by estrogeni
169 e analyzed the role of the nitric oxide (NO)/soluble guanylyl cyclase (sGC)/cGMP/cGMP-dependent prote
170 y activates a pool of oxidized and heme-free soluble guanylyl cyclase (sGC; see the related article b
171 ked whether the classical, nitric oxide (NO)-soluble guanylyl-cyclase (sGC)-cGMP pathway could modula
173 perties of NO synthase (NOS), as well as the soluble guanylyl cyclases (sGCs), which are the best cha
174 (ODQ, 5-20 microM), a selective inhibitor of soluble guanylyl cyclase, suppressed spontaneous swimmin
179 eptor-type guanylyl cyclases, the eukaryotic soluble guanylyl cyclases, the unicellular eukaryotic an
180 ion as coneurotransmitters, both stimulating soluble guanylyl cyclase to cause smooth muscle relaxati
181 h both NO and carbon monoxide (CO) stimulate soluble guanylyl cyclase to form cGMP, NO also S-nitrosy
182 o not appear to be mediated by activation of soluble guanylyl cyclase to produce cGMP, as these cells
183 through NO synthases, over interaction with soluble guanylyl cyclase, to eventual disposal as nitrit
186 on the ability of NO to access its receptor, soluble guanylyl cyclase, was explored by measuring cGMP
187 GC, indicating that particulate rather than soluble guanylyl cyclases were involved in iNOS inductio
188 M, SNP effects are probably mediated through soluble guanylyl cyclase, whereas in Sph the CNP effects
190 ons in the brain resembling localizations of soluble guanylyl cyclase, which is activated by CO.
191 ignal via cGMP that is generated by a NO and soluble guanylyl cyclase, while bradykinin B(2) receptor
192 evel NO signals for activating its receptor, soluble guanylyl cyclase, whilst avoiding adverse effect
193 butenyl)-L-ornithine (L-VNIO, 100 microM) or soluble guanylyl cyclase with 1H-[1, 2, 4]oxadiazolo[4,
194 osis was not attenuated by the inhibition of soluble guanylyl cyclase with ODQ, nor could apoptosis b
195 sphodiesterase inhibitors, by stimulation of soluble guanylyl cyclase with YC-1 or with exogenous dib
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