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1 AMP response requires mechanisms upstream of adenylyl cyclase.
2 ecifically, we hypothesize that AMP inhibits adenylyl cyclase.
3 the G-protein responsible for activation of adenylyl cyclase.
4 s measure pH via bicarbonate-sensing soluble adenylyl cyclase.
5 ich can specifically inhibit the activity of adenylyl cyclase.
6 te kinase M2 (PKM2) interaction with soluble adenylyl cyclase.
7 cium influx and Gi/o-dependent inhibition of adenylyl cyclase.
8 the beta(3a)-AR, caveolin-1, Galpha(s), and adenylyl cyclase.
9 ing to stimulation of G(i) and inhibition of adenylyl cyclase.
10 nt with reports that CO2 directly stimulates adenylyl cyclase.
11 ly rectifying potassium channels, as well as adenylyl cyclase.
12 to biological agents involving activation of adenylyl cyclase.
13 pha subunit of heterotrimeric G proteins and adenylyl cyclases.
14 ransgenic mice lacking calmodulin-stimulated adenylyl cyclases.
15 was restricted to the transmembrane class of adenylyl cyclases.
16 ic cAMP that is mediated by Ca(2+)-sensitive adenylyl cyclases.
17 ins, e.g. in histidine kinases and bacterial adenylyl cyclases.
18 is mediated by calcium/calmodulin-stimulated adenylyl cyclases.
19 ng (SOcAMPS) and activating Ca(2+) regulated adenylyl cyclases.
20 s long thought to be specifically coupled to adenylyl cyclases.
21 ck gene Npas2, and the clock-controlled gene adenylyl cyclase 1 (Adcy1) in a subset of retinal gangli
22 gh frequency of calcium input is filtered by adenylyl cyclase 1 and phosphodiesterases in this pathwa
25 lase LSD1 and the OR-dependent expression of adenylyl cyclase 3 (Adcy3) as requirements for initiatio
28 , whose synthesis is catalysed by the enzyme adenylyl cyclase 5 (AC5), which is itself regulated by t
29 ated basal ciliary cAMP level is a result of adenylyl cyclase 5 and 6 activity that depends on ciliar
31 this study, the fecal bacterial community of adenylyl cyclase 5 knock-out (AC5KO, n = 7) mice or thei
32 cells contains a protein complex comprising adenylyl cyclase 5/6 (AC5/6), A-kinase anchoring protein
34 tan and pasireotide, which indirectly reduce adenylyl cyclase 6 (AC6) activity, have hence proven eff
35 enerated intestinal epithelial cell-specific adenylyl cyclase 6 (AC6) knockout mice to study its role
37 roximal tubule-derived, PC1-knock-out cells, adenylyl cyclase 6 and 3 (AC6 and -3) are both expressed
38 heterotrimeric G-protein subunit G(s) alpha, adenylyl cyclase 6, and activation of the cAMP-regulated
40 d for chemoattractant-mediated activation of adenylyl cyclase 9 (AC9), which converts ATP into cAMP a
42 gnaling cascade leading to the activation of adenylyl cyclase A (ACA), the synthesis and secretion of
43 D2 receptor (D2R) to inhibit G(i/o)-mediated adenylyl cyclase, a recent study has shown that many APD
44 occur in mice lacking calmodulin-stimulated adenylyl cyclases, a mouse strain that learns but cannot
46 2 receptors that are linked to activation of adenylyl cyclase (AC) and an increase in cyclic adenosin
47 le cells, prostaglandin E2 (PGE2) stimulates adenylyl cyclase (AC) and attenuates the increase in int
48 ptake inhibitors, SSRIs) treatment increased adenylyl cyclase (AC) and BDNF gene expression in LCLs.
49 I-induced SA requires continuing activity of adenylyl cyclase (AC) and cAMP-dependent protein kinase
60 We have previously identified a subset of adenylyl cyclase (AC) isoforms that interact with Yotiao
62 th a G(alphas) inhibitor and an inhibitor of adenylyl cyclase (AC) prevented stimulating effects of O
65 n mammalian cells, an intramitochondrial CO2-adenylyl cyclase (AC)-cyclic AMP (cAMP)-protein kinase A
68 dorant receptor response was not mediated by adenylyl cyclase (AC)/cyclic nucleotide-gated (CNG) chan
69 anion exchanger 2 (Cl(-) /HCO3 (-) AE2), and adenylyl cyclase (AC)8 (proteins regulating large biliar
72 iological pacing using the Ca(2+)-stimulated adenylyl cyclase AC1 gene expressed alone or in combinat
75 reasons that remain unclear, whether type 5 adenylyl cyclase (AC5), 1 of 2 major AC isoforms in hear
79 atids and detailed studies of trypanosomatid adenylyl cyclases (ACs) and phosphodiesterases (PDEs) si
80 s, nanodomain clustering of Ca(2+)-sensitive adenylyl cyclases (ACs) drives oscillations of local cAM
82 ited cAMP levels after direct stimulation of adenylyl cyclases (ACs) with forskolin (FSK), as determi
83 eptors are responsible for the activation of adenylyl cyclases (ACs), which increase intracellular cy
85 cAMP is synthesized by one of 10 homologous adenylyl cyclases (ACs): nine transmembrane enzymes and
86 although salmeterol shows weak efficacy for adenylyl cyclase activation and G protein-coupled recept
87 rts demonstrating that signaling by PGE2 and adenylyl cyclase activation are associated with macropha
88 CB1b blockade by JD-5037 results in stronger adenylyl cyclase activation compared to rimonabant and i
90 h hormonal stimulation of cAMP generation by adenylyl cyclases (activation phase) and cAMP hydrolysis
91 al mu-opioid signaling through inhibition of adenylyl cyclase, activation of MAPK and G protein-gated
92 f PGI2 on stress fibres were mimicked by the adenylyl cyclase activator forskolin and prevented by in
95 Repeated microinjections of morphine or the adenylyl cyclase activator NKH477 into the vlPAG decreas
96 ntractile agonist acetylcholine (ACh) or the adenylyl cyclase activator, forskolin (FSK), a dilatory
98 thermore, we demonstrated that forskolin, an adenylyl cyclase activator, significantly increased the
99 ive against MEK2 cleavage by lethal toxin or adenylyl cyclase activity by edema toxin in human kidney
100 cyclase, partly due to reduced inhibition of adenylyl cyclase activity by pertussis toxin-sensitive G
101 cellular cAMP consistent with an increase in adenylyl cyclase activity for both mutants relative to w
102 to the field, CB1b is a potent regulator of adenylyl cyclase activity in peripheral metabolic tissue
103 DOR-KOR heteromer agonist 6'-GNTI inhibited adenylyl cyclase activity in vitro as well as PGE(2)-sti
106 tissues may be, in part, caused by enhanced adenylyl cyclase activity, but inhibition of cAMP degrad
107 has been of interest because the product of adenylyl cyclase activity, cAMP, is relevant to cilia-re
108 ed in mu agonist-induced G protein coupling, adenylyl cyclase activity, receptor internalization and
109 two compounds are equipotent for inhibiting adenylyl cyclase activity, these results suggest that Co
117 ntify that, in Fmr1 knockout neurons, type 1 adenylyl cyclase (Adcy1) mRNA translation is enhanced, l
119 lls (caSMCs) and caECs, resulting in soluble adenylyl cyclase Adcy10-dependent (sAC-dependent) increa
120 CD34(+) cell culture model, we show that the adenylyl cyclase agonist forskolin inhibits megakaryocyt
121 l because PGE2 could be substituted with the adenylyl cyclase agonist forskolin, and CCR8 expression
122 both the stimulatory G protein (Gs) for the adenylyl cyclase and arrestin pathways, synthetic ligand
123 ugh Galphas G-proteins and via activation of adenylyl cyclase and cAMP-dependent protein kinase, but
124 in) agonists to inhibit forskolin-stimulated adenylyl cyclase and increase mitogen-activated protein
125 educes the negative regulation by Galphai of adenylyl cyclase and its production of cAMP, independent
128 AR(2) causes Galphas-dependent activation of adenylyl cyclase and PKA, which activates TRPV4 and sens
130 ction potential through PAR(2) Inhibitors of adenylyl cyclase and protein kinase A (PKA) prevented th
131 is induced by neuronal activity via soluble adenylyl cyclase and protein kinase A (PKA) signaling.
132 that express a mutated PTH1R that activates adenylyl cyclase and protein kinase A (PKA) via Gsalpha
134 and stimulated neuronal hyperexcitability by adenylyl cyclase and protein kinase A-dependent mechanis
135 obutamine, reflecting its better coupling to adenylyl cyclase and the reliance of dopamine on dopamin
136 termined by the balance of cAMP synthesis by adenylyl cyclases and degradation by phosphodiesterases
137 ing subcellular targeting of cAMP-generating adenylyl cyclases and processes regulated by their compa
138 inase A isoform (PKAI) signaling pathway, as adenylyl-cyclase and PKAI inhibition prevented adenosine
139 sion in YY1(T372R) tumors included ADCY1 (an adenylyl cyclase) and CACNA2D2 (a Ca(2+) channel); both
140 ependence of the enzymes that generate cAMP (adenylyl cyclase) and degrade it (phosphodiesterase).
142 gulated cyclic nucleotide phosphodiesterase, adenylyl cyclase, and E. coli transcription factor FhlA
144 phs stimulated by forskolin, an activator of adenylyl cyclases, and by membrane-permeable cAMP analog
145 minal GAF (cGMP-specific phosphodiesterases, adenylyl cyclases, and FhlA) domain and two EAL motifs w
146 ir, where Rv0891c has sequence similarity to adenylyl cyclases, and Rv0890c harbors the NB-ARC-TPR-HT
147 TRPV4 currents in Xenopus laevis oocytes by adenylyl cyclase- and protein kinase A (PKA)-dependent m
148 on one of its cognate receptor, TAS2R43, and adenylyl cyclase; and (ii) reduced by homoeriodictyol (H
149 ue, Inda et al. show that different forms of adenylyl cyclase are activated at the plasma membrane ve
150 validation of 3 predicted relevant proteins, adenylyl cyclase-associated protein 1 (CAP1), SHC-transf
152 These 2 receptors have opposing actions on adenylyl cyclase because of differential G-protein coupl
154 falciparum through conditional disruption of adenylyl cyclase beta (ACbeta) and its downstream effect
155 fiers of cAMP signaling, the photo-activated adenylyl cyclase bPAC and the light-activated phosphodie
158 tal terminal segments enhanced activation of adenylyl cyclase by 50-75% and diminished activation of
159 mal cAMP resulting from direct activation of adenylyl cyclase by forskolin (15,689 +/- 7038% of contr
160 /- myocytes fail to respond to activation of adenylyl cyclase by forskolin, and the localized express
161 ensable, but Ras1 is found to associate with adenylyl cyclase Cac1 through the conserved Ras associat
163 mediate cAMP-induced stimulation of chimeric adenylyl cyclases, cAMP binding did not stimulate the PD
164 o reduced activity of the downstream cascade adenylyl cyclase-cAMP-PKA-cAMP response element-binding
168 component protective antigen (PA) and of the adenylyl cyclase catalytic moiety, edema factor (EF).
169 These results show that the upregulation of adenylyl cyclase caused by repeated vlPAG morphine admin
170 hese studies was to test the hypothesis that adenylyl cyclase contributes to opioid tolerance by modu
171 choline, dopamine, and adenosine signals via adenylyl-cyclase coupled GPCRs in shaping the dopamine-d
172 pase C-coupled D1R agonist (but not a D2R or adenylyl cyclase-coupled D1R agonist) decreased the pers
173 e cytosolic portion of the membrane-integral adenylyl cyclase Cya from Mycobacterium intracellulare i
177 -293 cells, ostensibly through inhibition of adenylyl cyclase, decreases intracellular levels of cAMP
178 blocked STa/GCC-dependent, but not forskolin/adenylyl cyclase-dependent, cystic fibrosis transmembran
180 ization consisting of an N-terminal putative adenylyl cyclase domain fused to a nucleotide-binding ad
182 rotein, followed by subsequent activation of adenylyl cyclase, elevation of cyclic AMP levels, and pr
184 R in a sequential manner, such as G protein, adenylyl cyclase, Epac-1 protein, and inositol 1,4,5-tri
185 rusion connecting the cGMP phosphodiesterase/adenylyl cyclase/FhlA (GAF) and phytochrome-specific (PH
186 ne form of the cyclic GMP phosphodiesterases/adenylyl cyclase/FhlA (GAF) domain from the cyanobacteri
187 for the photosensing cGMP phosphodiesterase/adenylyl cyclase/FhlA (GAF) domain from Thermosynechococ
188 ore buried within the cGMP phosphodiesterase/adenylyl cyclase/FhlA (GAF) domain, and a well-ordered h
189 es of the 23-kDa GAF (cGMP phosphodiesterase/adenylyl cyclase/FhlA) domain fragment of phytochrome fr
191 ivation of Gs, the stimulatory G protein for adenylyl cyclase, has long been a model system for GPCR
192 terol showed weak efficacy for activation of adenylyl cyclase; however, its efficacy in the complex d
194 This study used immunohistochemistry for adenylyl cyclase III (ACIII), a marker of primary cilia,
195 tivation of odorant receptors (ORs) leads to adenylyl cyclase III activation, cAMP increase, and open
196 2 and Gli3 repressors and early depletion of adenylyl cyclase III in neuroepithelial cilia, implicati
199 e of UDP-glucose for promoting inhibition of adenylyl cyclase in C6 glioma cells stably expressing th
201 r instance, expression of the Rutabaga (Rut) adenylyl cyclase in gamma neurons is sufficient to resto
202 queductal gray, nor a super-sensitization of adenylyl cyclase in the striatum, which are hallmarks of
204 ructure of Gs, the stimulatory G protein for adenylyl cyclase, in complex with the alpha2 adrenergic
205 t (expected to activate matrix-bound soluble adenylyl cyclase) increased intramitochondrial cAMP, but
206 RPV1 via activation of TRPA1, which involves adenylyl cyclase, increased cAMP, subsequent translocati
207 or (GPCR) that signals primarily through the adenylyl cyclase-inhibiting heterotrimeric G protein G(i
208 ex, implicating enhanced Galpha(i)-dependent adenylyl cyclase inhibition as a possible causative fact
210 n of G proteins with all Galphai/o subunits, adenylyl cyclase inhibition, and beta arrestin recruitme
211 otein activation, beta-arrestin recruitment, adenylyl cyclase inhibition, and extracellular signal-re
212 activated G-protein-dependent calcium flux, adenylyl cyclase inhibition, and the rapid activation of
213 r functional assays: ERK1/2 phosphorylation, adenylyl cyclase inhibition, calcium mobilization, and b
216 ocked by the CFTR inhibitor CFTR_inh172, the adenylyl cyclase inhibitor MDL 12330A, and the protein k
218 multiple G protein alpha subunits, including adenylyl cyclase-inhibitory (Galpha(i)) subunits and tho
222 rosclerosis triggers a de novo expression of adenylyl cyclase isoform 8 (AC8), associated with the pr
223 or more of the nine different transmembrane adenylyl cyclase isoforms that generate the cAMP signal
224 t Plin5 is phosphorylated, and activation of adenylyl cyclase leads to phosphorylation of Plin5, sugg
225 sticity was dependent on the Rutabaga type I adenylyl cyclase, linking cAMP-dependent plasticity to b
226 that for the structurally related membranous adenylyl cyclases (mACs) 1, 2, 5 and the purified mAC ca
228 f betaARs as well as Gi inhibition of type 1 adenylyl cyclase may underlie the experimental observati
229 brane-permeable 8Br-cAMP under inhibition of adenylyl cyclase-mediated cAMP production by MDL 12330A.
230 egion; a cytoplasmic HAMP (histidine kinase, adenylyl cyclases, methyl-accepting chemotaxis proteins,
231 otifs first identified in histidine kinases, adenylyl cyclases, methyl-accepting chemotaxis proteins,
232 er-Arnt-Sim) and poly-HAMP (histidine kinase-adenylyl cyclase-methyl-accepting chemotaxis protein-pho
233 ough the activation of phospholipase Cbeta-, adenylyl cyclase-, mitogen-activated protein kinase-, an
236 Par(2) deletion, LI-1, and inhibitors of adenylyl cyclase or protein kinase A (PKA) prevented the
237 roperties toward the beta(1)AR in either the adenylyl cyclase or the mitogen-activated protein kinase
238 rmone- and G protein-regulated transmembrane adenylyl cyclases or via the widely expressed and struct
240 tant residues for the enhanced activation of adenylyl cyclase, partly due to reduced inhibition of ad
241 T6) receptor constitutively activates the Gs/adenylyl cyclase pathway in various cell types, includin
242 nistic actions of the canonical G protein -> adenylyl cyclase pathway that is initiated by G-protein-
244 uction of cAMP (G protein-coupled receptors, adenylyl cyclases, phosphodiesterases (PDEs)), and recep
246 ciated with a decrease in the sensitivity of adenylyl cyclase production of cAMP to inhibitory Galpha
249 in NMJ growth and plasticity, including the adenylyl cyclase Rutabaga, the Ig-CAM Fasciclin II, the
250 work we used a HAMP containing mycobacterial adenylyl cyclase, Rv3645, as a reporter enzyme in which
251 cAMP sources, involving the atypical soluble adenylyl cyclase (sAC) in addition to transmembrane aden
253 addition, the cAMP-producing enzyme soluble adenylyl cyclase (sAC) is expressed in pigment cells, an
254 study, significant overexpression of soluble adenylyl cyclase (sAC), an alternative source of cAMP, w
255 increased expression and activity of soluble adenylyl cyclase (sAC), an evolutionarily conserved bica
256 e Ca(2+)/HCO(3)(-)-sensitive enzyme, soluble adenylyl cyclase (sAC), links Ca(2+) influx in human cor
260 d the expression and function of the soluble adenylyl cyclase (sAC, ADCY10) in CNS retinal ganglion c
261 mimics the action of the endogenous soluble adenylyl cyclase (SACY) that is required for motility an
262 These findings indicate that cilia-dependent adenylyl cyclase signaling represses the Hedgehog pathwa
263 nonical negative interaction at the level of adenylyl cyclase signaling, to a strong recruitment of b
264 reabsorption in the collecting duct through adenylyl cyclase-stimulated cyclic AMP, which exists as
265 stimulation (G(s)) or inhibition (G(i/o)) of adenylyl cyclase, stimulation of potassium channel curre
267 ic receptor (beta2AR) bound to the G protein adenylyl cyclase stimulatory G protein (Gs) captured the
268 nction of the encoded protein, Galphaolf, an adenylyl-cyclase-stimulatory G-protein highly enriched i
272 s the enzyme to a specific, light-stimulated adenylyl cyclase that catalyzes the formation of cAMP fr
273 l of c-di-AMP is modulated by activity of di-adenylyl cyclase that produces c-di-AMP and phosphodiest
277 ylyl cyclases synthesize cAMP, transmembrane adenylyl cyclases (tmACs), and soluble adenylyl cyclase
280 oups converge on the same signaling cascade--adenylyl cyclase to cAMP to protein kinase A--but with o
282 creased functional coupling of Galpha(s) and adenylyl cyclase to increase intracellular cyclic adenos
283 FSI axon terminals and negatively couple to adenylyl cyclase to induce a long-term depression of GAB
284 of an activated C-Raf reduces sensitivity of adenylyl cyclase to opioids in nonexcitable HEK293 cells
285 n lipid rafts, couples less effectively with adenylyl cyclase to produce cAMP, and this is reversed b
286 m channels, while in turn, calcium activates adenylyl cyclases to produce more cAMP-PKA signaling.
289 lous DM(high)-VL(low) expression gradient of adenylyl cyclase type 3 appears, which coincides with al
295 To assess this, we studied mice deficient in adenylyl cyclase type VI specifically in the principal c
296 nctions to inhibit the production of cAMP by adenylyl cyclase upon Hh stimulation, thus maximizing si
298 xperiments revealed that acute activation of adenylyl cyclase with forskolin increased the frequency