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1 ion of a competitive inhibitor of a receptor guanylyl cyclase.
2 vitro, demonstrating that it is a functional guanylyl cyclase.
3 ssion of NF-kappaB and activation of soluble guanylyl cyclase.
4 ein-coupled receptors, adenylyl cyclase, and guanylyl cyclase.
5 f cGMP in response to nitric oxide-activated guanylyl cyclase.
6 way and the subsequent activation of soluble guanylyl cyclase.
7 ndothelial nitric-oxide synthase and soluble guanylyl cyclase.
8 of NO synthase and subsequent activation of guanylyl cyclase.
9 taining the synaptic localization of soluble guanylyl cyclase.
10 ndothelial nitric oxide synthase and soluble guanylyl cyclase.
11 extent, by the direct stimulation of soluble guanylyl cyclase.
12 a multidomain, membrane-associated receptor guanylyl cyclase.
13 h, among other functions, stabilizes soluble guanylyl cyclase.
14 but not natriuretic peptide (NP)-stimulated guanylyl cyclase.
15 s (GCAPs) bind and regulate retinal membrane guanylyl cyclase 1 (RetGC1) but not natriuretic peptide
16 erization domain of a human retinal membrane guanylyl cyclase 1 (RetGC1) linked to autosomal dominant
24 o uroguanylin in the CNS, which can activate guanylyl cyclase 2C (GUCY2C) receptors in the brain to r
25 ic actions, as the endogenous ligand for the guanylyl cyclase 2C receptor has revealed a new system i
27 effects were blocked by inhibition of either guanylyl cyclase A receptor or cyclic guanosine monophos
28 The two main receptors of NP, membrane-bound guanylyl cyclases A and B (GC-A and GC-B), mediate the e
30 t was shown that NPs, via their cGMP-forming guanylyl cyclase-A (GC-A) receptor and cGMP-dependent ki
31 Atrial natriuretic peptide (ANP) via its guanylyl cyclase-A (GC-A) receptor participates in regul
33 rtension decreases urine output, and second, guanylyl cyclase-A (GC-A), the primary signaling recepto
36 HF serums were active and generated cGMP via guanylyl cyclase-A receptors; however, the 180-minute sa
43 and cone photoreceptors by calcium-sensitive guanylyl cyclase activating proteins (GCAP1 and GCAP2) i
44 activity is modulated by the calcium-binding guanylyl cyclase activating proteins (GCAP1 and GCAP2).
45 etGC1 and RetGC2 isozymes using mice lacking guanylyl cyclase activating proteins GCAP1 and GCAP2 and
47 9C or E155G mutations of the retGC modulator guanylyl cyclase-activating protein 1 (GCAP-1), which pr
49 ackground light; similar effects are seen in guanylyl cyclase-activating protein knockout (GCAPs(-/-)
52 ane guanylyl cyclase 1 (RetGC1) regulated by guanylyl cyclase-activating proteins (GCAPs) controls ph
54 icial effects of both nitric oxide-sensitive guanylyl cyclase activation and inhibition of the cGMP-d
55 ing, leading to NO production and subsequent guanylyl cyclase activation and K(ATP) channel opening i
56 al NMDARs and NOS stimulation and subsequent guanylyl cyclase activation that probably occurred in pe
57 important role in NO generation and soluble guanylyl cyclase activation under hypoxic conditions, wi
60 th Exisulind, sulindac sulfide, OSI-461, the guanylyl cyclase activator YC-1, or the cell-permeable c
61 in distal human PASMCs treated with soluble guanylyl cyclase activators (nitric oxide donors and BAY
62 tors (VPAC2 and NPR-C), inhibit adenylyl and guanylyl cyclase activities, and stimulate cAMP-specific
63 uced dephosphorylation of NPR2 decreases its guanylyl cyclase activity in growth plate chondrocytes i
64 y changes, but the absence of GCAP2 affected guanylyl cyclase activity in two ways; (a) the maximal r
67 xposed to green light, whereas inhibition of guanylyl cyclase activity negatively affects fungal phot
69 in 20 min, LH treatment results in decreased guanylyl cyclase activity of NPR2, as determined in the
71 y Ca(2+)-dependent binding of recoverin, (2) guanylyl cyclase activity via Ca(2+)-dependent GCAP prot
72 CAP1 and GCAP2, confer Ca(2+) sensitivity to guanylyl cyclase activity, but the importance and the co
73 The protein exhibits robust light-dependent guanylyl cyclase activity, whereas a truncated form lack
75 oso-N-acetyl-DL-penicillamine) and a soluble guanylyl cyclase agonist (YC-1) mimicked AMPA effect in
76 es an effector domain such as an adenylyl or guanylyl cyclase, all encoded in a single protein as a t
77 UCY1A3 encodes the alpha1 subunit of soluble guanylyl cyclase (alpha1-sGC), and CCT7 encodes CCTeta,
82 imulatory role of NOS is mediated by soluble guanylyl cyclase and results from a cGMP-dependent stimu
83 cAMP receptor protein (CRP) is linked to the guanylyl cyclase and when deleted is deficient in cyst d
85 all previously uncharacterized receptor-type guanylyl cyclases and find them to be highly biased but
86 total of 27 gcy genes encoding receptor-type guanylyl cyclases and of 7 gcy genes encoding soluble gu
87 erotrimeric G proteins but is independent of guanylyl cyclases and the previously identified cGMP-ind
88 s issue, report direct communication between guanylyl cyclases and the Rac-p21-activated kinase (PAK)
89 s, harbors a catalytic center diagnostic for guanylyl cyclases and the recombinant AtPNP-R1 is capabl
90 porters, nitric oxide (NO) synthase, soluble guanylyl cyclase, and ATP-sensitive potassium (KATP) cha
92 phosphorylation and inactivation of the NPR2 guanylyl cyclase, and cGMP hydrolysis is increased by ac
93 ing pathway involving nitric oxide synthase, guanylyl cyclase, and cGMP-dependent protein kinase (PKG
94 e roles of endothelium-derived vasodilators, guanylyl cyclase, and potassium channels were examined i
97 find that >41% (11/27) of all receptor-type guanylyl cyclases are expressed in the ASE gustatory neu
98 dely distributed across all kingdoms whereas guanylyl cyclases are generally thought to be restricted
99 g membrane-integral and soluble adenylyl and guanylyl cyclases, are central components in a wide rang
101 C-type natriuretic peptide activation of guanylyl cyclase B (GC-B), also known as natriuretic pep
102 ceptor for C-type natriuretic peptide (CNP), guanylyl cyclase B (GC-B, also known as Npr2 or NPR-B),
104 structure of human BNP to activate GC-A and guanylyl cyclase-B (GC-B), which is not reduced in heart
105 tor 3 and inactivating mutations in the NPR2 guanylyl cyclase both cause severe short stature, but ho
106 naling proteins, including eucaryal receptor guanylyl cyclases, but its function remains obscure.
109 ginine methyl ester) and blockade of soluble guanylyl cyclase (by ODQ; 1H-1,2,4-oxadiazolo[4,3-a]quin
115 rgeting the intestinal cancer mucosa antigen guanylyl cyclase C (GCC) and its effect on inflammatory
117 tems, and the bacterial enterotoxin receptor guanylyl cyclase C (GCC), the principle source of cGMP i
118 ic tumors all express a unique surface-bound guanylyl cyclase C (GCC), which binds the diarrheagenic
120 nuation of the colonic cell surface receptor guanylyl cyclase C (GUCY2C) that occurs due to loss of i
122 enovirus (Ad5) combination regimen targeting guanylyl cyclase C (GUCY2C), a receptor expressed by int
123 endogenous ligands for the tumor suppressor guanylyl cyclase C (GUCY2C), disrupting a network of hom
125 prior to defining the baseline expression of guanylyl cyclase C mRNA, a marker for colorectal cancer,
126 ntrol of cGMP levels and that membrane-bound guanylyl cyclases can be critically modulated by other r
127 gether with Ca(2+)-dependent acceleration of guanylyl cyclase, can successfully account for changes i
129 g 8-bromo-cGMP, as well as by the NO-soluble guanylyl cyclase-cGMP signaling inhibitor thrombospondin
132 AY-41-2272 converts the CO adduct of soluble guanylyl cyclase (CO-sGC) enzyme from a low- to high-out
134 ts in target cells by binding to specialized guanylyl cyclase-coupled receptors, resulting in cGMP ge
137 tion of retinal arterioles via activation of guanylyl cyclase; cyclooxygenase plays a relatively mino
138 cretes cGMP when developing cysts and that a guanylyl cyclase deletion strain fails to synthesize cGM
139 n modification, biologically through soluble guanylyl-cyclase-dependent modulation of the MMP-9/TIMP-
140 e identified a link between impaired soluble-guanylyl-cyclase-dependent nitric oxide signalling and m
142 ion of the cyclase activity, we isolated the guanylyl cyclase domain from Escherichia coli with (GCwC
144 eight different receptor-type, transmembrane guanylyl cyclases (encoded by gcy genes), which are expr
145 uanylyl cyclase C (GUCY2C), a membrane-bound guanylyl cyclase expressed in intestinal epithelial cell
146 segment of a natriuretic peptide receptor A guanylyl cyclase failed to bind GCAPs, but replacing its
147 nsory neurons (OSNs) expressing the receptor guanylyl cyclase GC-D, the cyclic nucleotide-gated chann
148 PSM2), RAP1GAP, and Gbeta5; cGMP modulators: guanylyl cyclase (GC) 1alpha1, GC1beta1, phosphodiestera
150 pr1 promoter activity and greatly stimulated guanylyl cyclase (GC) activity of the receptor protein i
151 activation of the intestinal receptor-enzyme guanylyl cyclase (GC) C, triggers an acute, watery diarr
155 and MyD88-dependent recruitment of platelet guanylyl cyclase (GC) toward the plasma membrane, follow
156 MP-receptive mechanisms and the inhibitor of guanylyl cyclase (GC), LY-83,583, on sleep in rats.
158 hosphorylation is required for activation of guanylyl cyclase (GC)-A, also known as NPR-A or NPR1, by
159 gical effects in cells largely by activating guanylyl cyclase (GC)-coupled receptors, leading to cGMP
163 ions of phosphodiesterase (PDE6) and retinal guanylyl cyclases (GCs), and mutations in genes that dis
164 uses PAK to directly activate transmembrane guanylyl cyclases (GCs), leading to increased cellular c
168 rect inhibitors of an NRE-localized receptor-guanylyl-cyclase, GCY-8, which synthesizes cyclic guanos
169 After stimulation with nitric oxide, soluble guanylyl cyclase generates cGMP, which induces vasodilat
171 hyperphosphorylation occurs through soluble guanylyl cyclase/guanosine 3',5'-cyclic monophosphate si
176 on by the ligand NPPC, NPR2, the predominant guanylyl cyclase in follicular somatic cells, produces c
178 cyclases and of 7 gcy genes encoding soluble guanylyl cyclases in the complete genome sequence of C.
180 induced airway relaxation was resistant to a guanylyl cyclase inhibitor (ODQ) and a protein kinase G
181 ine dihydrochloride (1400W) and the specific guanylyl cyclase inhibitor 1-H (1, 2, 4)oxadiazolo[4,3-a
182 -nitro-L-arginine methyl ester (L-NAME), the guanylyl cyclase inhibitor 1H- [1,2,4]oxadiazolo[4,3-a]q
183 hylimidazoline-1-oxyl-3-oxide (PTIO) but not guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]qu
184 Porcine leaflets exposed to the soluble guanylyl cyclase inhibitor ODQ increased osteocalcin and
185 mediated depolarizations were blocked by the guanylyl cyclase inhibitor ODQ indicating involvement of
188 adiazolo-[4,3-a]quinoxalin-1-one) (a soluble guanylyl cyclase-inhibitor, Rp-8-(4-chlorophenylthio)-gu
190 Ps(-/-)) rods, indicating that regulation of guanylyl cyclase is not necessary for at least a part of
192 lation of cGMP synthesis by retinal membrane guanylyl cyclase isozymes (RetGC1 and RetGC2) in rod and
193 nthesis in photoreceptor by retinal membrane guanylyl cyclase isozymes (RetGC1 and RetGC2) to expedit
194 ugh H(2)S does not directly activate soluble guanylyl cyclase, it maintains a tonic inhibitory effect
195 wn cells and agonists for either adenylyl or guanylyl cyclase, it was found that PDE1B2 predominantly
196 ice that lack NO-GC specifically in SMCs (SM-guanylyl cyclase knockout [GCKO]), ICCs (ICC-GCKO), or b
197 NP is a critical discriminator of binding to guanylyl cyclase-linked but not clearance natriuretic pe
200 in the granulosa cells by the transmembrane guanylyl cyclase natriuretic peptide receptor 2 (NPR2) i
201 natriuretic peptide (CNP), its receptor, the guanylyl cyclase natriuretic peptide receptor 2 (Npr2),
202 granulosa cells, where it is produced by the guanylyl cyclase natriuretic peptide receptor 2 (NPR2).
203 eted disruption of the Npr1 gene (coding for guanylyl cyclase/natriuretic peptide receptor A (NPRA))
204 rial and brain natriuretic peptides activate guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NP
206 the application of a nitric oxide-sensitive guanylyl cyclase (NO-sGC) receptor antagonist, a NOS inh
207 ow that one of these molecules, the receptor guanylyl cyclase Npr2, is required for bifurcation of th
208 hermore, inhibition of the NO target soluble guanylyl cyclase or of the cGMP effector kinase protein
210 3-a]quinoxalon-1-one, a potent inhibitor for guanylyl cyclase, or 1,2-bis(2-aminophenoxy)ethane-N,N,N
211 that release nitric oxide, stimulate soluble guanylyl cyclase, or activate cGMP-dependent protein kin
212 all kingdoms of life, e.g. in human retinal guanylyl cyclase, our findings may be significant for ma
214 luding the insulin, TGF-beta, serotonin, and guanylyl cyclase pathways; however, the sensory processe
215 expression levels of particulate (membrane) guanylyl cyclases (pGC) and cGMP-specific phosphodiester
217 nic mutation carriers contained less soluble guanylyl cyclase protein and consequently displayed redu
218 3-kinase, endothelial nitric-oxide synthase, guanylyl cyclase, protein kinase G (PKG), and the mitoch
219 The effect of CORM-2 was not prevented by guanylyl-cyclase, protein kinase G, or thioredoxin inhib
220 e cytoplasmic Ca2+ concentration, activating guanylyl cyclase, raising cyclic GMP concentration, open
222 se (eNOS) by directly activating its soluble guanylyl cyclase receptor, rescued blood vessel function
223 inhibitors of NO synthase (NOS) and soluble guanylyl cyclase, respectively, abolished tadalafil indu
224 5'-cyclic monophosphate ([cGMP]i) by soluble guanylyl cyclase, resulting in fast onset and long-lasti
225 xide that retrogradely activated presynaptic guanylyl cyclase, resulting in the presynaptic expressio
227 hat change the Ca(2+) sensitivity of retinal guanylyl cyclase (retGC) can result from an increase in
228 al for normal expression of retinal membrane guanylyl cyclase (RetGC) in photoreceptor cells, blocks
229 is an EF-hand protein that activates retinal guanylyl cyclase (RetGC) in photoreceptors at low free C
230 that inhibit retinal photoreceptor membrane guanylyl cyclase (retGC) in the dark when they bind Ca(2
231 (2+) sensor protein that accelerates retinal guanylyl cyclase (RetGC) in the light and decelerates it
232 depend on Ca(2+)-regulated retinal membrane guanylyl cyclase (RetGC), comprised of two isozymes, Ret
236 The GUCY2D gene encodes retinal membrane guanylyl cyclase (RetGC1), a key component of the photot
239 utations in the AFD-expressed gcy-8 receptor guanylyl cyclase (rGC) gene result in defects in the exe
241 the observation that multiple receptor-type guanylyl cyclases (rGCs), encoded by the gcy genes, and
242 onstrate the effect of NO donors and soluble guanylyl cyclase (sGC) activators in differentiation of
244 established endogenous modulator of soluble guanylyl cyclase (sGC) activity, but physiological, stru
246 es that the functional properties of soluble guanylyl cyclase (sGC) are affected not only by the bind
247 dentified the alpha1-subunit gene of soluble guanylyl cyclase (sGC) as a novel androgen-regulated gen
248 nsertion is key during maturation of soluble guanylyl cyclase (sGC) because it enables sGC to recogni
249 es with the oxidation of the heme of soluble guanylyl cyclase (sGC) critically implicated in some of
251 nine (NMMA); 300 or 500 microM) or a soluble guanylyl cyclase (sGC) inhibitor (1H-[1,2,4]oxadiazolo[4
252 ell volume that was abolished by the soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,
253 -arginine methyl ester; 30 mg/kg), a soluble guanylyl cyclase (sGC) inhibitor [1H-(1, 2, 4) oxadiazol
254 either a nitric oxide scavenger or a soluble guanylyl cyclase (sGC) inhibitor diminished the benefici
255 Diatomic ligand discrimination by soluble guanylyl cyclase (sGC) is paramount to cardiovascular ho
258 MP levels in this pathway, including soluble guanylyl cyclase (sGC) itself, the NO -activated form of
259 and cGMP in the above effects using soluble guanylyl cyclase (sGC) or adenylate cyclase (AC) specifi
262 d neuronal systems via activation of soluble guanylyl cyclase (sGC), a heme-containing heterodimer.
263 ch encodes the alpha1 subunit of the soluble guanylyl cyclase (sGC), a key enzyme in the nitric oxide
264 They were tested for activation of soluble guanylyl cyclase (sGC), a key enzyme in the NO/cGMP sign
266 nal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC), and can be mimicked by the nitri
267 the major downstream effector of NO, soluble guanylyl cyclase (sGC), in the superficial dorsal horn o
270 through activation of its receptor, soluble guanylyl cyclase (sGC), leading to elevation of intracel
271 noxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase (sGC), or Rp-8-Br-cGMP, an inhibitor of
272 presence of inhibitors selective for soluble guanylyl cyclase (sGC), PKG, calmodulin, CaMKII or ERK1/
273 ural homology to the beta subunit of soluble guanylyl cyclase (sGC), suggesting a NO sensing function
274 homologous to the central region in soluble guanylyl cyclase (sGC), the main receptor for nitric oxi
275 ular mechanism of desensitization of soluble guanylyl cyclase (sGC), the NO receptor, has long remain
277 ly vasoactive through stimulation of soluble guanylyl cyclase (sGC), which produces the second messen
278 to determine whether NO activates a soluble guanylyl cyclase (sGC)-cyclic guanosine monophosphate (c
284 ed the role of the nitric oxide (NO)/soluble guanylyl cyclase (sGC)/cGMP/cGMP-dependent protein kinas
285 tes a pool of oxidized and heme-free soluble guanylyl cyclase (sGC; see the related article beginning
286 her the classical, nitric oxide (NO)-soluble guanylyl-cyclase (sGC)-cGMP pathway could modulate Ca(2)
289 s, evolutionary diversification of primitive guanylyl cyclase signaling pathways allows GUCY2C to coo
291 at this toxin is a dual soluble adenylyl and guanylyl cyclase that results in intracellular cAMP and
292 peptide receptor B (NPR-B) are transmembrane guanylyl cyclases that catalyze the synthesis of cGMP in
293 ructural diversity of microbial adenylyl and guanylyl cyclases, the enzymes that synthesize cAMP and
294 olar concentrations of nitric oxide activate guanylyl cyclase to produce cGMP, which has diverse phys
295 canonical 5'-3' DNA polymerases and adenylyl/guanylyl cyclases, two enzyme families known to use a tw
300 e conditional expression of either wild-type guanylyl cyclase, which synthesizes cGMP, or a mutated g
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