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1 iven by the hsp90 chaperone machinery and by soluble guanylyl cyclase.
2 I)PPIX remains four coordinate when bound to soluble guanylyl cyclase.
3 Four-coordinate metalloporphyrins activate soluble guanylyl cyclase.
4 quires endothelial nitric oxide synthase and soluble guanylyl cyclase.
5 old rats do not express the beta subunit of soluble guanylyl cyclase.
6 receptors act by NO-mediated stimulation of soluble guanylyl cyclase.
7 endothelial nitric oxide synthase (NOS) and soluble guanylyl cyclase.
8 signaling pathways mediated by a CO receptor soluble guanylyl cyclase.
9 oprotective effect is mediated by activating soluble guanylyl cyclase.
10 ansfer of NO-ferroheme and activation of apo-soluble guanylyl cyclase.
11 smaller extent, by the direct stimulation of soluble guanylyl cyclase.
12 ex, which, among other functions, stabilizes soluble guanylyl cyclase.
13 d suppression of NF-kappaB and activation of soluble guanylyl cyclase.
14 ERK pathway and the subsequent activation of soluble guanylyl cyclase.
15 is via endothelial nitric-oxide synthase and soluble guanylyl cyclase.
16 by maintaining the synaptic localization of soluble guanylyl cyclase.
17 show similarity to the regulatory domain of soluble guanylyl cyclases.
19 nor was partially blocked by an inhibitor of soluble guanylyl cyclase, 1H-[1,2,4]oxadiazolo[4,3, -a]q
21 2 receptors to stimulate cGMP production via soluble guanylyl cyclase activation and absorption throu
22 vailability of NO would be too low to elicit soluble guanylyl cyclase activation in the presence of b
23 play an important role in NO generation and soluble guanylyl cyclase activation under hypoxic condit
25 transient cGMP response upon particulate or soluble guanylyl cyclase activation, while the cGMP resp
27 measured in distal human PASMCs treated with soluble guanylyl cyclase activators (nitric oxide donors
28 and cAMP-dependent mechanism for modulating soluble guanylyl cyclase activity in pituitary cells.
30 (S-nitroso-N-acetyl-DL-penicillamine) and a soluble guanylyl cyclase agonist (YC-1) mimicked AMPA ef
33 3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, also blocked the effects of ni
38 The stimulatory role of NOS is mediated by soluble guanylyl cyclase and results from a cGMP-depende
40 of Dictyostelium discoideum, a heterodimeric soluble guanylyl cyclase, and a homodimeric membrane gua
41 te transporters, nitric oxide (NO) synthase, soluble guanylyl cyclase, and ATP-sensitive potassium (K
42 esent study, we determined the role of cGMP, soluble guanylyl cyclase, and protein kinase G in the po
43 and by sodium nitroprusside, an activator of soluble guanylyl cyclase, and was potentiated by a cGMP-
44 ts is due to the lack of the beta subunit of soluble guanylyl cyclase, and we speculate that this def
46 ups in both Ni(II)- and Cu(II)-reconstituted soluble guanylyl cyclase are consistent with a substanti
48 The mechanism was due to the activation of soluble guanylyl cyclase because 8-bromo-cyclic GMP acti
49 ffects of CO in this study were mediated via soluble guanylyl cyclase, because 1H-(1,2,4)oxadiazole (
51 by N(G)-nitro-L-arginine methyl ester and of soluble guanylyl cyclase by 1H-[1,2,4]oxadiazolo[4,3,-a]
52 d receptors stimulate nitric oxide-sensitive soluble guanylyl cyclase by increasing intracellular Ca(
54 tro-L-arginine methyl ester) and blockade of soluble guanylyl cyclase (by ODQ; 1H-1,2,4-oxadiazolo[4,
55 MP analog 8-bromo-cGMP, as well as by the NO-soluble guanylyl cyclase-cGMP signaling inhibitor thromb
56 ulator BAY-41-2272 converts the CO adduct of soluble guanylyl cyclase (CO-sGC) enzyme from a low- to
57 ese data support a model where activation of soluble guanylyl cyclase correlates with the absence of
58 nisms through which NO generally acts is the soluble guanylyl cyclase-cyclic GMP (sGC-cGMP) pathway.
59 d protein modification, biologically through soluble guanylyl-cyclase-dependent modulation of the MMP
60 , we have identified a link between impaired soluble-guanylyl-cyclase-dependent nitric oxide signalli
62 .By blocking the activity of NO synthase and soluble guanylyl cyclase enzymes after training, we prov
65 ht to be mediated by the action of NO on the soluble guanylyl cyclase (GC) in the smooth muscle and s
67 ric oxide synthase (NOS) and the NO receptor-soluble guanylyl cyclase (GC), the activation of which l
68 eviously demonstrated that the NO-stimulated soluble guanylyl cyclase (GC1), which produces cGMP, als
70 iven pRb hyperphosphorylation occurs through soluble guanylyl cyclase/guanosine 3',5'-cyclic monophos
72 contains three genes that code for atypical soluble guanylyl cyclases: Gyc-88E, Gyc-89Da, and Gyc-89
76 uanylyl cyclases and of 7 gcy genes encoding soluble guanylyl cyclases in the complete genome sequenc
77 imulated fluid absorption was blocked by the soluble guanylyl cyclase inhibitor 1-H-[1,2,4]oxadiazolo
78 n viable cells, which was not blocked by the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[
79 romo-cyclic GMP activated PI3 kinase and the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[
80 this lusitropic effect was attenuated by the soluble guanylyl cyclase inhibitor 1H:-[1,2,4]oxadiazolo
82 ,4)oxadiazole (4,3-alpha) quinoxaline-1-one (soluble guanylyl cyclase inhibitor) completely reversed
83 e to anoxic conditions and is blocked by the soluble guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo
84 These effects were inhibited by LY 83583, a soluble guanylyl cyclase inhibitor, and mimicked by 8-Br
88 ,2,4]-oxadiazolo-[4,3-a]quinoxalin-1-one) (a soluble guanylyl cyclase-inhibitor, Rp-8-(4-chlorophenyl
89 he presence of various phosphodiesterase and soluble guanylyl cyclase inhibitors, confirming that G(s
91 GMP; though H(2)S does not directly activate soluble guanylyl cyclase, it maintains a tonic inhibitor
93 by the additional presence of inhibitors of soluble guanylyl cyclase (LY83583) or protein kinase G (
94 xpression of Foxp3 in MBP-primed T cells via soluble guanylyl cyclase-mediated production of cGMP.
95 ther and how cardiomyocyte NO-sensitive GC1 (soluble guanylyl cyclase) mediates female-specific, adap
96 icroM 8-Bromo-cGMP), and (iii) inhibition of soluble guanylyl cyclase (ODQ (1H-[1,2,4,]oxadiazolo(4,3
97 e (NO) synthesis, L-NNA, and an inhibitor of soluble guanylyl cyclase, ODQ, greatly enhanced colonic
100 agents that release nitric oxide, stimulate soluble guanylyl cyclase, or activate cGMP-dependent pro
101 e conclude that NO production, activation of soluble guanylyl cyclase, or changes in intracellular cG
103 rom digenic mutation carriers contained less soluble guanylyl cyclase protein and consequently displa
105 ors of phosphodiesterase 5 or stimulators of soluble guanylyl cyclase rapidly enhanced multiple prote
106 e synthase (eNOS) by directly activating its soluble guanylyl cyclase receptor, rescued blood vessel
107 n-1-one, inhibitors of NO synthase (NOS) and soluble guanylyl cyclase, respectively, abolished tadala
108 sine 3',5'-cyclic monophosphate ([cGMP]i) by soluble guanylyl cyclase, resulting in fast onset and lo
109 , we demonstrate the effect of NO donors and soluble guanylyl cyclase (sGC) activators in differentia
112 y firmly established endogenous modulator of soluble guanylyl cyclase (sGC) activity, but physiologic
115 e isoforms (ACs 1-9), a structurally related soluble guanylyl cyclase (sGC) and a soluble AC (sAC).
117 indicates that the functional properties of soluble guanylyl cyclase (sGC) are affected not only by
118 e have identified the alpha1-subunit gene of soluble guanylyl cyclase (sGC) as a novel androgen-regul
119 Heme insertion is key during maturation of soluble guanylyl cyclase (sGC) because it enables sGC to
120 of recombinant nitric oxide (NO)-stimulated soluble guanylyl cyclase (SGC) by Ca2+ was demonstrated.
121 r diseases with the oxidation of the heme of soluble guanylyl cyclase (sGC) critically implicated in
122 Nitric oxide (NO)-unresponsive forms of soluble guanylyl cyclase (sGC) exist naturally and in di
124 nce that treatment with NO donors stimulates soluble guanylyl cyclase (sGC) in the MCC, and as a resu
125 9A mRNA expression closely resembles that of soluble guanylyl cyclase (sGC) in the rat brain, suggest
126 l-L-arginine (NMMA); 300 or 500 microM) or a soluble guanylyl cyclase (sGC) inhibitor (1H-[1,2,4]oxad
127 ase in cell volume that was abolished by the soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadi
128 -nitro-L-arginine methyl ester; 30 mg/kg), a soluble guanylyl cyclase (sGC) inhibitor [1H-(1, 2, 4) o
129 nt with either a nitric oxide scavenger or a soluble guanylyl cyclase (sGC) inhibitor diminished the
140 e of nitric oxide (NO) in the stimulation of soluble guanylyl cyclase (sGC) is well established, but
141 ts of cGMP levels in this pathway, including soluble guanylyl cyclase (sGC) itself, the NO -activated
142 of cAMP and cGMP in the above effects using soluble guanylyl cyclase (sGC) or adenylate cyclase (AC)
143 have shown that the levels of expression of soluble guanylyl cyclase (sGC) or cGMP-dependent protein
145 iated by nitric oxide (NO), which stimulates soluble guanylyl cyclase (sGC) production of the second
146 blots for endothelial NO synthase (eNOS) and soluble guanylyl cyclase (sGC) revealed reduced eNOS exp
148 e monophosphate (cGMP) synthesis by forms of soluble guanylyl cyclase (sGC) that do not respond to NO
150 pression of the alpha1 and beta1 subunits of soluble guanylyl cyclase (sGC) was directly and specific
152 cular and neuronal systems via activation of soluble guanylyl cyclase (sGC), a heme-containing hetero
153 s in the brain largely through activation of soluble guanylyl cyclase (sGC), a heterodimer comprised
154 s in the brain largely through activation of soluble guanylyl cyclase (sGC), a heterodimer comprising
155 1A3, which encodes the alpha1 subunit of the soluble guanylyl cyclase (sGC), a key enzyme in the nitr
158 proximately 9% contained the beta subunit of soluble guanylyl cyclase (sGC), a major target of NO.
159 of neuronal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC), and can be mimicked by t
162 tion of the major downstream effector of NO, soluble guanylyl cyclase (sGC), in the superficial dorsa
164 by localizing the expression and activity of soluble guanylyl cyclase (SGC), its principal molecular
165 ignaling through activation of its receptor, soluble guanylyl cyclase (sGC), leading to elevation of
167 ,3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase (sGC), or Rp-8-Br-cGMP, an inhi
168 in the presence of inhibitors selective for soluble guanylyl cyclase (sGC), PKG, calmodulin, CaMKII
169 ted optic nerve, nitric oxide (NO) activates soluble guanylyl cyclase (sGC), resulting in a selective
170 h structural homology to the beta subunit of soluble guanylyl cyclase (sGC), suggesting a NO sensing
171 n yet is homologous to the central region in soluble guanylyl cyclase (sGC), the main receptor for ni
172 he molecular mechanism of desensitization of soluble guanylyl cyclase (sGC), the NO receptor, has lon
175 clinically vasoactive through stimulation of soluble guanylyl cyclase (sGC), which produces the secon
176 tudies determined that the nitric oxide (NO)-soluble guanylyl cyclase (sGC)-cGMP pathway plays a sign
177 tly increased in cells that had a functional soluble guanylyl cyclase (sGC)-cGMP signaling pathway an
178 onducted to determine whether NO activates a soluble guanylyl cyclase (sGC)-cyclic guanosine monophos
179 ta(3)-adrenoceptors (beta(3)-ARs) coupled to soluble guanylyl cyclase (sGC)-dependent production of t
191 s that investigated the regulation of the NO/soluble guanylyl cyclase (sGC)/cGMP pathway by estrogeni
193 e analyzed the role of the nitric oxide (NO)/soluble guanylyl cyclase (sGC)/cGMP/cGMP-dependent prote
194 lex with glutamate NMDA receptors (NMDA-Rs), soluble guanylyl cyclase (sGC, the NO receptor), and PSD
195 y activates a pool of oxidized and heme-free soluble guanylyl cyclase (sGC; see the related article b
196 ked whether the classical, nitric oxide (NO)-soluble guanylyl-cyclase (sGC)-cGMP pathway could modula
199 perties of NO synthase (NOS), as well as the soluble guanylyl cyclases (sGCs), which are the best cha
201 (ODQ, 5-20 microM), a selective inhibitor of soluble guanylyl cyclase, suppressed spontaneous swimmin
206 eptor-type guanylyl cyclases, the eukaryotic soluble guanylyl cyclases, the unicellular eukaryotic an
207 ion as coneurotransmitters, both stimulating soluble guanylyl cyclase to cause smooth muscle relaxati
208 h both NO and carbon monoxide (CO) stimulate soluble guanylyl cyclase to form cGMP, NO also S-nitrosy
209 o not appear to be mediated by activation of soluble guanylyl cyclase to produce cGMP, as these cells
210 through NO synthases, over interaction with soluble guanylyl cyclase, to eventual disposal as nitrit
213 on the ability of NO to access its receptor, soluble guanylyl cyclase, was explored by measuring cGMP
214 GC, indicating that particulate rather than soluble guanylyl cyclases were involved in iNOS inductio
215 ed formation of NO species and activation of soluble guanylyl cyclase, where xanthine oxidoreductase
216 M, SNP effects are probably mediated through soluble guanylyl cyclase, whereas in Sph the CNP effects
218 ons in the brain resembling localizations of soluble guanylyl cyclase, which is activated by CO.
219 ignal via cGMP that is generated by a NO and soluble guanylyl cyclase, while bradykinin B(2) receptor
220 evel NO signals for activating its receptor, soluble guanylyl cyclase, whilst avoiding adverse effect
221 butenyl)-L-ornithine (L-VNIO, 100 microM) or soluble guanylyl cyclase with 1H-[1, 2, 4]oxadiazolo[4,
222 osis was not attenuated by the inhibition of soluble guanylyl cyclase with ODQ, nor could apoptosis b
223 sphodiesterase inhibitors, by stimulation of soluble guanylyl cyclase with YC-1 or with exogenous dib