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1 PKA activation also promotes survival of murine neutroph
2 PKA activation potentiated MF glutamatergic responses of
3 PKA phosphorylates TCF4 directly and a PKA phosphorylati
4 PKA stimulates cellular gene expression by phosphorylati
5 PKA was performed using a 2-tissue, 3-compartment irreve
12 and serum deprivation, ABA stimulates, in a PKA- and cADPR-dependent fashion, the mitogen-activated
13 ose-stimulated insulin secretion (GSIS) in a PKA-dependent manner and prevented saturated fatty acid-
14 neuronal networks appear to be affected in a PKA-dependent manner, whereas behaviorally important hip
15 uronal networks appeared to be affected in a PKA-dependent manner, whereas hippocampal-PFC projection
17 uolar membranes revealed that ML1 mediates a PKA-activated conductance on TV membranes that is requir
19 fic to AKAP150, as viral overexpression of a PKA-binding deficient mutant of AKAP150 also impairs coc
21 in the presence of insulin, treatment with a PKA-selective agonist mimicked the ability of glucagon t
22 nhibit Nrg1III by limiting protein kinase A (PKA) activation, which is required to initiate myelinati
24 a SvJ129 background, cAMP/protein kinase A (PKA) and AMP-activated protein kinase (AMPK) signaling p
25 res the activation of both protein kinase A (PKA) and the GTPase Ras, and is induced upon the activat
26 e monophosphate (cAMP) and protein kinase A (PKA) are important mediators and regulators of apoptosis
29 ociated with a decrease of protein kinase A (PKA) catalytic subunit alpha (Calpha) expression both at
33 Ser133 phosphorylation by protein kinase A (PKA) is a well-characterized CREB activation mechanism.
36 ced activation of the cAMP/protein kinase A (PKA) pathway by melanocortin 2 receptor (MC2R), leading
37 positive modulators of the protein kinase A (PKA) pathway, inhibited by the CB1R antagonist rimonaban
39 regulated kinase (ERK) and protein kinase A (PKA) play important roles in LTP and spine structural pl
41 DEs actively targeting the protein kinase A (PKA) R-subunit through formation of a PDE-PKAR-cyclic ad
43 s support a major role for protein kinase A (PKA) signaling in shaping the FLC gene expression landsc
45 iple signals that activate protein kinase A (PKA) signaling, which positively regulates neutrophil su
49 n yeast, glucose activates protein kinase A (PKA) to accelerate aging by inhibiting transcription fac
50 PRKAR1beta), activation of protein kinase A (PKA), and phosphorylation of alpha4-integrin on serine 9
51 of protein kinase G (PKG), protein kinase A (PKA), phosphodiesterase 3B (PDE3B), and a membrane-perme
52 I PDZ motif with SAP97 and protein kinase A (PKA)-anchoring protein (AKAP) 5, which anchor the recept
53 effects were mediated by a protein kinase A (PKA)-dependent enhancement of presynaptic GABA release.
54 sma membrane and increased protein kinase A (PKA)-dependent protein phosphorylation in purified medul
55 -1R activation promoting a protein kinase A (PKA)-dependent signaling cascade leading to phosphorylat
56 aled that GD1a activated a protein kinase A (PKA)-dependent signaling pathway and increased phosphory
58 ts were caused by impaired protein kinase A (PKA)-mediated phosphorylation because exogenous PKA rest
59 ers the relief of Ig20 and protein kinase A (PKA)-mediated phosphorylation of Ser-2152, thereby dynam
69 ediated through the activation of common (AC/PKA) and distinct (PLC/PKC, intra-/extra-cellular calciu
72 eta-Adrenergic stimulation rapidly activated PKA, which led to the phosphorylation of ATGL and HSL an
74 echniques revealed that catalytically active PKA holoenzymes remained intact within the cytoplasm.
76 In this study, pharmacokinetic analysis (PKA) of (18)F-FMISO dynamic PET extended to 3 h after in
77 ngs indicate that the parameters of anchored PKA holoenzyme action are much more restricted than orig
78 ush-pull between direct TRPV1 activation and PKA-dependent regulation of channel inactivation, with p
79 e competition between calmodulin binding and PKA phosphorylation and the differential effects of this
81 othesis that C. sakazakii increases cAMP and PKA activation in experimental NEC resulting in increase
82 ased reporters for the detection of cAMP and PKA activity in intact cells and we establish that the s
84 y, these observations indicate that cAMP and PKA phosphorylation are associated with increased apopto
85 Similarly, increased intestinal cAMP and PKA phosphorylation were demonstrated in a rat pup model
87 ubstrates and a cross-talk between CDPK1 and PKA, and show the role of CDPK1 in parasite invasion.
88 ved sensors, we succeeded in imaging ERK and PKA activation in single dendritic spines during structu
91 between the control of ARPP-16 by MAST3 and PKA that creates a mechanism whereby cAMP mediates PP2A
93 Under hyperglycemia, cAMP production and PKA activity were markedly increased as a result of gluc
95 processes downstream of PKA, we deleted both PKA catalytic subunits using CRISPR-Cas9, followed by a
96 line, which displayed marked defects in both PKA activation and isoproterenol-induced ATGL translocat
100 e binding of 14-3-3zeta to MAP2c enhanced by PKA-mediated phosphorylation is likely to influence micr
103 spond to the same signal (phosphorylation by PKA) but have different downstream effects, indicating a
107 nisms revealed that activation of PPP1R1A by PKA phosphorylation at Thr35, and subsequent PP1 binding
108 horylation, and this effect was prevented by PKA inhibitors, suggesting the involvement of PKA in ROL
112 ERKs is transient and rapidly terminated by PKA phosphorylation of the Raf isoforms C-Raf and B-Raf.
113 folding protein for Protein Kinases A and C (PKA and PKC, respectively), AKAP facilitates phosphoryla
115 e more compartmentalized regulation of cAMP, PKA, and EPAC, they have limited ability to link this re
118 l-d-aspartate receptors and weakened by cAMP-PKA-potassium channel signaling in dendritic spines.
120 tively, these data demonstrate that the cAMP-PKA pathway plays a key role in epigenetic regulation of
122 o study the effect of modulation of the cAMP-PKA-dependent pathway on ICAM-4 receptor activation.
123 a-adrenergic receptor and activates the cAMP-PKA-dependent pathway, caused a significant increase in
125 ough ADORA2A and ADORA2B receptors in a cAMP/PKA pathway-dependent mechanism to induce V-ATPase-depen
126 HD, and that measurements of sleep and cAMP/PKA could be prodromal indicators of disease, and serve
128 induces local Gs-protein activation and cAMP/PKA signaling at a critical position near the nucleus, w
129 also involved activation of Galphas and cAMP/PKA, and inhibition of increase in exchange protein dire
130 nt to participation of the cGMP/PKG and cAMP/PKA/Epac (exchange protein directly activated by cAMP) d
132 study, we interrogate the complexity in cAMP/PKA-MAPK/ERK1&2 crosstalk by using multi-parameter biose
133 tically, the absence of Cav-1 increased cAMP/PKA signaling in EC, as indicated by elevated phosphoryl
138 ATF4 expression and that activation of cAMP/PKA and PI3K/Akt/mTORC1 mediates the effect of glucagon
139 induced ADP is blocked by inhibitors of cAMP/PKA signaling, insensitive to pertussis toxin or beta-ar
140 rization was dependent on inhibition of cAMP/PKA signaling, whereas reversal of Gbetagamma-stimulated
141 phoproteomes of the functional pools of cAMP/PKA/EPAC that are regulated by specific cAMP-PDEs (the P
142 his PGI2 increase appeared to stimulate cAMP/PKA pathways, contributing to the enhanced lipolysis in
149 rule out a role for all conserved consensus PKA phosphorylation sites in alpha1C in beta-adrenergic
150 cocaine-seeking behavior by amplifying D1DR/PKA-dependent AMPA transmission in the nucleus accumbens
151 ion is also compromised since cAMP-dependent PKA activity is enhanced, increasing the probability of
153 ated to identify a causal network describing PKA signaling that explains vasopressin-mediated regulat
154 The ERK2 site is downstream of a direct PKA site in the Rap1GAP, Sipa1l1, that indirectly inhibi
156 ulated of these being NR4A2 and NR4A3 Direct PKA activation by the site-selective PKA agonist pair N6
160 9 proteins were discovered as substrates for PKA, but the function of PKA phosphorylation is unknown.
161 findings suggest the existence of a glucose-PKA pathway that inactivates conserved zinc finger stres
162 or --> Gs --> adenylate cyclase --> cAMP --> PKA --> cAMP response element-binding protein pathway me
171 ated in vitro by multiple kinases, including PKA and PKC, and pharmacological activation of these kin
173 KA-specific activator, 6-Bnz-cAMP, increased PKA activity (6.8 +/- 2.0 mean fold versus vehicle; P =
174 e signalling via erythrocyte ADORA2B induces PKA phosphorylation, ubiquitination and proteasomal degr
175 locking receptor internalization, inhibiting PKA II/interfering with its Golgi/TGN localization, sile
178 e, but only later in life, and this involves PKA, its catalytic subunit Calpha, and the Wnt/beta-cate
179 IL-1Ra upregulation elicited by LPS alone is PKA-independent, whereas the rolipram-enhanced response
180 knockdown of cAMP-dependent protein kinase (PKA) activity in prestalk cells reduced stalk gene induc
181 tion by cyclic AMP-dependent protein kinase (PKA) underlies key cellular processes, including sympath
183 increases in cAMP-dependent protein kinase (PKA), or the activity of exchange protein activated by c
185 ection and from AKAP-knock-out mice had less PKA activity, GRK2 Ser-685 phosphorylation, and GRK2 pla
187 ted CREB at Ser271 but not Ser133; likewise, PKA phosphorylated CREB at Ser133 but not Ser271, sugges
188 A-kinase anchoring proteins (AKAPs) localize PKA to AMPARs leading to enhanced phosphorylation of Glu
189 The lack of EH-myomesin, combined with low PKA-mediated phosphorylation of myofilament proteins and
191 ages of two donors to simultaneously measure PKA and ERK1&2 kinase activities in the same cellular lo
192 utants indicated that impaired AKAP-mediated PKA scaffolding significantly reduces DOR-GRK2 associati
193 tivation of intracellular second messengers, PKA and PKCepsilon, indicating that HMWH-induced antihyp
194 ortant component of the inflammatory milieu, PKA internalizes Slack channels from the DRG membrane, r
195 (PKA) biosensor allowed us to resolve minute PKA activity microdomains on the plasma membranes of liv
197 -activated cross-linking approach to monitor PKA subunit interactions with temporal precision in livi
206 and treatment with endogenous activators of PKA, including adenosine and prostaglandin E2, results i
209 ng an undiscovered mode for amplification of PKA activity by cAMP-mediated sequestration of the R-sub
212 To probe the quantitative attributes of PKA dynamics in the yeast Saccharomyces cerevisiae, we d
215 ement of the apparent activation constant of PKA or shielding of PKA from bulk cytosolic cAMP via loc
216 o identify signaling processes downstream of PKA, we deleted both PKA catalytic subunits using CRISPR
217 nstead, we have identified other features of PKA signaling for reducing catalytic subunit diffusion a
219 ased apoptosis in NEC and that inhibition of PKA activation protects against apoptosis and experiment
224 These results presented a novel mechanism of PKA and IkappaB pathway, which may be targeted for treat
228 , using two independent optical reporters of PKA activity in acute mouse hippocampus slices, we show
230 lls and we establish that the sensitivity of PKA to cAMP is almost twenty times lower when measured i
231 t activation constant of PKA or shielding of PKA from bulk cytosolic cAMP via localization of the enz
232 which influenced the downstream signaling of PKA pathway, including altered the expression of MKP-1.
234 vels of catalytic and regulatory subunits of PKA were increased by glucocorticoids in wild-type mice.
238 isplatin-induced DNA damage was dependent on PKA-mediated phosphorylation of ATR on S435 which promot
240 Phosphorylation of Kelch-like 3 by PKC or PKA downstream of AngII or vasopressin signaling, respec
245 eonine, which is predicted to be a potential PKA phosphorylation site by at least one prediction tool
246 oes not require any combination of potential PKA phosphorylation sites conserved in human, guinea pig
248 pancreatic islets, fasting conditions reduce PKA and mTOR activity and induce Sox2 and Ngn3 expressio
249 fasting or glucose restriction (GR) regulate PKA and AMP-activated protein kinase (AMPK) to protect a
254 These findings suggest that AKAP scaffolds PKA to increase plasma membrane targeting and phosphoryl
255 at the plasma membrane in neurons, scaffolds PKA to target proteins to mediate downstream signal.
256 Direct PKA activation by the site-selective PKA agonist pair N6/8-AHA (8-AHA-cAMP and N6-MB-cAMP) an
261 of CFTR current activation, we propose that PKA phosphorylation of the R domain is enabled by its in
262 neutrophil gene array studies, we show that PKA activation upregulates a significant number of apopt
263 tro pharmacological experiments suggest that PKA dysregulation in the mPFC underlies cognitive dysfun
264 to refute the recently proposed theory that PKA catalytic subunits remain tethered to regulatory sub
266 ifferential phosphorylation of STEP61 at the PKA sites, Ser-160 and Ser-221 regulates the affinity of
269 fibronectin aggregates was abolished by the PKA inhibitor H89, whereas the effect of GD1a was mimick
270 , to study the properties of feedback in the PKA signaling network and dissect the nonintuitive dynam
272 phosphosites that enhance the effects of the PKA/CKI kinases on SMO accumulation, its localization at
273 ntial therapeutic value of inhibition of the PKA/PPP1R1A/PP1 pathway in the treatment of primary and
277 ptors increases HSC survival in part via the PKA-mediated induction of the cAMP response element-bind
282 IL-27 does not appear to be mediated through PKA, exchange protein activated by cAMP, PI3K, or MAPKs.
285 , the P2204L mutant is readily accessible to PKA, promoting ligand-independent phosphorylation on Ser
286 This cognitive deficit is consecutive to PKA deregulation in the mPFC that prevents Ophn1 KO mice
287 tions," wherein cAMP is locally delivered to PKA at supersaturating concentrations to cause uncouplin
288 of a downstream transcriptional response to PKA activation in the neutrophil, and that they positive
289 y was to define transcriptional responses to PKA activation and to delineate the roles of these facto
293 m spiny neurons but that dopamine acting via PKA inactivates ARPP-16 leading to selective potentiatio
295 ERK phosphorylation on Thr(202)/Tyr(204) was PKA-dependent, but MEK(Ser(217)/Ser(221)) phosphorylatio
296 Consequently, unlike in WT filamin, where PKA-mediated Ser-2152 phosphorylation is ligand-dependen
297 ed stalk gene induction by c-di-GMP, whereas PKA activation bypassed the c-di-GMP requirement for sta
300 pho-RhoA was localised in actin nodules with PKA type II and a number of other phosphorylated PKA sub
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