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1 aling, and activation of cAMP-dependent PKA (protein kinase A).
2 erlotinib was independent of cAMP, cGMP, and protein kinase A.
3 hosphorylation of NMDA and AMPA receptors by protein kinase A.
4 cycle regulator, and the metabolic regulator protein kinase A.
5 pendently of the classical effector of cAMP, protein kinase A.
6 rocess is associated with fast activation of protein kinase A.
7 ibitory hexapeptide GRGDSP and inhibition of protein kinase A.
8 o study the cAMP binding domain A (CBD-A) of Protein kinase A.
9 neurons is induced by neuronal activity and protein kinase A.
10 n axonal specification through activation of protein kinase A.
11 n the extensive cytosolic domain of STIM1 by protein kinase A.
12 ssociation with 14-3-3 proteins and involves protein kinase A.
13 obligatory dependence on phosphorylation by protein kinase A.
14 equent stimulation of CFTR by cAMP-dependent protein kinase A.
15 s dependent on Pg phosphorylation at S665 by protein kinase A.
16 transcription factor that acts downstream of protein kinase A.
17 ith forskolin and H89 to activate or inhibit protein kinase A (a family of enzymes whose activity dep
18 ardiac myosin-binding protein-C (cMyBP-C) by protein kinase A accelerates the kinetics of force devel
19 2 on PAR-4 expression, whereas cicaprost via protein kinase A activation counteracted this effect.
20 t the molecular level, capacitation requires protein kinase A activation, changes in membrane potenti
23 involving both an increase in cAMP-dependent protein kinase A activity and the GLI3R to GLI3A ratio.
24 wed that this approach can be used to detect protein kinase A activity in lysate from HEK293 cells.
25 protein level, female ARVMs exhibited higher protein kinase A activity, consistent with pathway enric
26 drenergic receptor Abs, as well as increased protein kinase A activity, suggesting a potential mechan
27 maps of the kinase domain of cAMP-dependent protein kinase A allow for a molecular explanation for t
28 demonstrate that Shp2 is a component of the protein kinase A anchoring protein (AKAP)-Lbc complex.
31 ate kinases, including SAP97 and PSD-95, and protein kinase A-anchoring protein (AKAP) 5 in the plasm
33 x of patients, upregulated activities of the protein kinase A and C pathways and changes in neurotran
34 virus genomes, we show that costimulation of protein kinase A and C-delta signaling cascades in conju
35 c stimulation or increased pacing because of protein kinase A and CaMKIIdelta phosphorylations of cMy
36 mote human Th17 responses via cAMP-dependent protein kinase A and caspase-1/inflammasome-dependent IL
37 fically Ca2+/calmodulin activated kinase II, protein kinase A and exchange protein activated by cAMP
38 lipolysis, Perilipin 5 is phosphorylated by protein kinase A and forms transcriptional complexes wit
39 eta2 -adrenergic receptor phosphorylation at protein kinase A and G-protein receptor kinase sites in
40 3 antagonizes TGFbeta-mediated activation of protein kinase A and inhibition of Protein kinase B (AKT
41 Pre-LTP also involves adenylyl cyclase and protein kinase A and is expressed via a mechanism involv
42 ugh the signaling of protein kinases such as protein kinase A and p38 mitogen-activated protein kinas
43 ncreased phosphorylation of phospholamban by protein kinase A and relief of sarco/endoplasmic reticul
46 etal muscle, and brain and phosphorylated by protein kinases A and C at Ser-68 and Ser-63, respective
47 on (e.g. by Pho85-Pho80, Cdc28-cyclin B, and protein kinases A and C) and dephosphorylation (e.g. by
48 t S373, S365, and S368, well-known Cx43 Akt, protein kinase A, and protein kinase C phosphorylation s
51 by beta-adrenergic receptors, cyclic AMP and protein kinase A as revealed by pharmacological experime
52 nhibition of beta2-adrenergic receptor 2 and protein kinase A, as well as silencing of hypoxia-induci
53 xpression levels of AKAP7, a gene encoding a protein kinase A-binding scaffolding molecule, were sign
55 d through ATP binding and phosphorylation by protein kinase A, but fails to operate in cystic fibrosi
57 ccurs via the cyclic adenosine monophosphate-protein kinase A (cAMP-PKA)-dependent signaling pathway.
59 1 was not activated through the classic cAMP/protein kinase A (cAMP/PKA) pathway or via the AKT, MK2,
62 tifying cancer-associated mutations in human protein kinases, a class of signaling proteins known to
63 solution properties, as little as 0.1 U/muL protein kinase A could be detected in short reaction tim
64 ipal component analysis of available GRK and protein kinase A crystal structures to identify their do
65 67 kDa laminin-receptor (67LR) resulting in protein kinase A dependent activation of protein phospha
66 roduction of cyclic adenosine monophosphate, protein kinase A-dependent activation of the extracellul
67 Although beta2AR stimulation in DC induces protein kinase A-dependent cAMP-responsive element-bindi
73 cular level, metoprolol expectedly decreased protein kinase A-dependent phospholamban and ryanodine r
76 of CPG2 binding to the actin cytoskeleton by protein kinase A directly impacts recruitment of EndoB2
77 nge is caused by cocaine-exacerbated D1-cAMP/protein kinase A dopamine signaling in pyramidal neurons
78 TP induction is caused by sensitized D1-cAMP/protein kinase A dopamine signaling in pyramidal neurons
79 optimal linker allows its phosphorylation by protein kinase A during bacterial co-expression and subs
80 allows for convergent activation of PDK1 and protein kinase A during paired stimulation to initiate c
81 probability >0.3) in the absence of ATP and protein kinase A, each normally required for CFTR activi
82 nels are not characteristically activated by protein kinase A even though the phosphorylation levels
83 s of renal tubule epithelial cells; elevates protein kinase A, extracellular signal-regulated kinases
84 e the hydrogels with a peptide substrate for protein kinase A further enhanced the sensitivity of the
85 d receptor kinases (GRKs) are members of the protein kinase A, G, and C families (AGC) and play a cen
86 l stiffness, which was partially restored by protein kinase A in both mild and severe RV dysfunction.
87 protein-coupled receptor kinase/arrestin and protein kinase A in salmeterol-mediated desensitization
88 r282, and Ser302) that are phosphorylated by protein kinase A in the m-domain of cMyBP-C were replace
89 ines produced upon LPS challenge occurs in a protein kinase A-independent manner and, rather, is asso
96 t the phosphorylation of the T389 residue by protein kinase A is mediated by the association of plasm
97 ntact myocytes and selective displacement of protein kinase A isoforms, we demonstrate that the antih
99 o and found that a positive feedback loop on protein kinase A mediated by the AMP-activated protein k
103 and cyclic adenosine monophosphate-dependent protein kinase A-mediated hyperphosphorylation of RYR2-S
105 a-adrenergic stimulation as a consequence of protein kinase A-mediated phosphorylation or as a result
106 sed imaging reveals that activity-driven and Protein Kinase A-mediated PS1 phosphorylation at three d
107 2 activation inhibited protein kinase C- and protein kinase A-mediated sensitization processes throug
108 t-evoked temporal Ca(2+) release profile and protein kinase A modulation of Ca(2+) release are marked
109 tion coupling is cAMP-dependent, neither the protein kinase A nor the exchange protein directly activ
110 the kidney by a direct stimulatory action of protein kinase A on the plasma membrane trafficking and
112 calization mutant, or a mutant lacking the 5 protein kinase A or C phosphorylation sites interfered w
113 ease in intracellular cAMP, independently of protein kinase A or exchange protein directly activated
117 block of signalling pathways involving ATP, protein kinase A or the formation of lipid rafts, and do
118 o increased by pharmacological activation of protein kinases A or C and decreased by inhibition of th
119 mplicated the cyclic adenosine monophosphate/protein kinase A pathway as well as FosB and dynorphin-B
122 es for NDI that target the canonical VP/cAMP/protein kinase A pathway have so far proven ineffective,
124 arrow-derived macrophages, PGE2 via the cAMP/protein kinase A pathway is potently inducing IL-1beta t
125 lic adenosine monophosphate (cAMP)-dependent protein kinase A pathway to inhibit HIV-1 activation and
126 e cardiac function, particularly through the protein kinase A pathway, and could potentially be respo
127 action of GnIH on the adenylate cyclase/cAMP/protein kinase A pathway, suggesting a common inhibitory
132 n (Pg) and direct phosphorylation at S665 by protein kinase A: Pg deficiency as well as overexpressio
134 Biochemical measurements confirmed that protein kinase A phosphorylated ser273, ser282, and ser3
135 PKD and was associated with higher levels of protein kinase A-phosphorylated (Ser133) cAMP-responsive
138 ction between PSD95 and KV1 channels enables protein kinase A phosphorylation of KV1 channels in cVSM
139 These findings provide initial evidence that protein kinase A phosphorylation of KV1 channels is enab
141 yR1 from Tric-a KO mice are not activated by protein kinase A phosphorylation, demonstrating a defect
143 at cAMP inhibits myometrial contractions via protein kinase A (PKA) activation, but this has yet to b
149 -activated current was not affected when the protein kinase A (PKA) activity was blocked with H89, or
150 T generate an ITF that depends on persistent protein kinase A (PKA) activity, whereas an ITF produced
152 f PDE3B KO mice on a SvJ129 background, cAMP/protein kinase A (PKA) and AMP-activated protein kinase
154 e differentially modulated by cAMP-dependent protein kinase A (PKA) and exchange protein directly act
155 ) is a cytosolic scaffolding protein binding protein kinase A (PKA) and glycogen synthase kinase 3bet
157 a physical and functional connection between protein kinase A (PKA) and Gpr161 (an orphan GPCR) signa
158 a2 integrin activation on PMNs by activating protein kinase A (PKA) and inhibiting activation of the
160 potentiation requires the activation of both protein kinase A (PKA) and the GTPase Ras, and is induce
161 Cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) are important mediators and regul
163 hat cAMP promotes phosphorylation of S897 by protein kinase A (PKA) as well as increases the phosphor
164 rdiac troponin I (cTnI) is phosphorylated by protein kinase A (PKA) at sites S23/S24, located at the
166 We generate a novel genetically encoded protein kinase A (PKA) biosensor anchored onto the myofi
167 ion of the A kinase activity reporter (AKAR) protein kinase A (PKA) biosensor as an example-first in
168 lin-dependent protein kinase II (CaMKII) and protein kinase A (PKA) both in vitro and in heterologous
170 ased; this was associated with a decrease of protein kinase A (PKA) catalytic subunit alpha (Calpha)
171 ties of a BrS-associated SCN5A mutation in a protein kinase A (PKA) consensus phosphorylation site, R
172 a regulatory subunit of cyclic AMP-dependent protein kinase A (PKA) display reduced adiposity and res
173 I(1-39)), is a target for phosphorylation by protein kinase A (PKA) during beta-adrenergic stimulatio
178 gulates signal transduction through cAMP and protein kinase A (PKA) in melanocytes, is a major inheri
179 ring development and impacts the activity of Protein Kinase A (PKA) in striatal spiny projection neur
180 ophosphate, and the subsequent activation of protein kinase A (PKA) induce a mesenchymal-to-epithelia
181 ation of Ih observed in SNI neurons, whereas protein kinase A (PKA) inhibition further promoted this
187 rylation of the regulatory domain of CFTR by protein kinase A (PKA) is required for its channel activ
189 ngoing cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) levels, strongly limiting SK chan
192 s of the spatially and temporally controlled protein kinase A (PKA) network in diverse eukaryotic mod
193 ity can be regulated by phosphorylation with protein kinase A (PKA) or AKT, which, in turn, inhibits
194 We show that cAMP signaling through the protein kinase A (PKA) pathway activates Src homology do
195 ormone (ACTH)-induced activation of the cAMP/protein kinase A (PKA) pathway by melanocortin 2 recepto
196 n was emulated by positive modulators of the protein kinase A (PKA) pathway, inhibited by the CB1R an
202 racellular signal-regulated kinase (ERK) and protein kinase A (PKA) play important roles in LTP and s
204 is initiated by PDEs actively targeting the protein kinase A (PKA) R-subunit through formation of a
205 The regulation of L-type Ca(2+) channels by protein kinase A (PKA) represents a crucial element with
206 TG) mice expressing non-phosphorylatable TnI protein kinase A (PKA) residues (i.e. serine to alanine
209 al glucagon-like peptide-1 receptor (Glp-1r)-protein kinase A (Pka) signaling and a neuronal-mediated
210 t disease-related mutations that impair cAMP protein kinase A (PKA) signaling are present within the
213 lincRNA signatures support a major role for protein kinase A (PKA) signaling in shaping the FLC gene
214 ministration of an agent that activates cAMP-protein kinase A (PKA) signaling led to attenuation of p
215 has been ascribed to the cAMP/cAMP-dependent protein kinase A (PKA) signaling pathway in retinoid tre
217 ls respond to multiple signals that activate protein kinase A (PKA) signaling, which positively regul
224 ormally, the scaffold protein AKAP1 recruits protein kinase A (PKA) to the outer mitochondrial membra
226 ed PTH1R that activates adenylyl cyclase and protein kinase A (PKA) via Gsalpha but not phospholipase
227 reased spark-to-spark delays; (2) activating protein kinase A (PKA) with forskolin accelerated amplit
228 rylation of tyrosine residues by Etk/Bmx and protein kinase A (PKA) within an assembled signaling com
230 ry subunit 1beta (PRKAR1beta), activation of protein kinase A (PKA), and phosphorylation of alpha4-in
231 how that JMJD1A is phosphorylated at S265 by protein kinase A (PKA), and this is pivotal to activate
232 ctivate three cAMP sensors downstream of AC [protein kinase A (PKA), exchange protein activated by cA
233 s with inhibitors of protein kinase G (PKG), protein kinase A (PKA), phosphodiesterase 3B (PDE3B), an
234 anchoring protein AKAP79/150 interacts with protein kinase A (PKA), protein kinase C (PKC), and prot
235 rapid induction (4 h compared with 3 d); (2) protein kinase A (PKA), rather than PKCepsilon, dependen
237 upled receptor that signals through cAMP and protein kinase A (PKA), regulates pigmentation, adaptive
238 phide between regulatory-RIalpha subunits of protein kinase A (PKA), which stimulates PKA-dependent E
239 r flight heart rate (HR) increases depend on protein kinase A (PKA)- and calmodulin kinase II (CaMKII
240 lated phosphoprotein of 32 kDa (DARPP-32), a protein kinase A (PKA)-activated and calcineurin (CaN)-d
241 e C-terminal type I PDZ motif with SAP97 and protein kinase A (PKA)-anchoring protein (AKAP) 5, which
242 AGM is enriched for expression of targets of protein kinase A (PKA)-cAMP response element-binding pro
243 eurons, and these effects were mediated by a protein kinase A (PKA)-dependent enhancement of presynap
247 licle-stimulating hormone (FSH) promotes the protein kinase A (PKA)-dependent phosphorylation of insu
249 esicles to the plasma membrane and increased protein kinase A (PKA)-dependent protein phosphorylation
250 neurons, with GLP-1R activation promoting a protein kinase A (PKA)-dependent signaling cascade leadi
251 ity profiling revealed that GD1a activated a protein kinase A (PKA)-dependent signaling pathway and i
252 major calcium signaling molecule, and report protein kinase A (PKA)-independent CFTR activation by ca
253 g brown adipocytes through cyclic AMP (cAMP)/protein kinase A (PKA)-mediated lipolysis and fatty acid
254 tractile impairments were caused by impaired protein kinase A (PKA)-mediated phosphorylation because
255 his scaffolding protein regulates a shift in protein kinase A (PKA)-mediated phosphorylation events u
257 to this site triggers the relief of Ig20 and protein kinase A (PKA)-mediated phosphorylation of Ser-2
258 nd that CL-II phosphorylation is promoted by protein kinase A (PKA)-mediated phosphorylation of Smo C
260 show that GIE deformability is regulated by protein kinase A (PKA)-mediated phosphorylation of the S
261 transcription principally by activating the protein kinase A (PKA)-targeted transcription factors.
274 beta-cell function is mediated through cAMP/protein kinase A (PKA)/nephrin-dependent pathways, we fo
275 oform of the second messenger cAMP-dependent protein kinase A (PKAalpha) rapidly phosphorylates USP20
276 rm capacitation, the immediate activation of protein kinase A plays a pivotal role, promoting the sub
278 mutations in either the catalytic subunit of protein kinase A (PRKACA) or the guanine nucleotide-bind
280 rotein 1 (Drp1) activation via inhibition of protein kinase A-regulated S637 phosphorylation, resulti
282 was associated with decreased expression of protein kinase A regulatory subunit 1beta (PRKAR1beta),
283 ucleotide binding domains (NBD1 and NBD2) by protein kinase A results in increased channel open proba
284 nd systems: cAMP-bound regulatory subunit of Protein Kinase A (RIalpha) and IBMX-bound phosphodiester
285 its a remarkable degree of conservation with protein kinase A (root mean square deviation = 1.8 A), i
286 onserved cyclic nucleotide-binding domain of protein kinase A's (PKA) regulatory subunit as a prototy
287 yclic nucleotide-gated channels and the cAMP/protein kinase A signaling axis in promoting hyperexcita
288 ermine that ethanol activates a Galphas-cAMP-protein kinase A signaling pathway in IL2 neurons to sti
289 platelet aggregation by modulating the cAMP-protein kinase A signaling pathway, suggesting that MRP4
290 r, enhancement of particular aspects of cAMP/protein kinase A signaling seems to be beneficial for th
291 ward calcium-protein kinase C and cyclic AMP-protein kinase A signaling, which open potassium channel
292 -adrenergic receptor (beta2 AR) at both the protein kinase A site serine 261/262 and the G-protein-c
293 HSL) at S565, with higher phosphorylation at protein kinase A sites S563 and S660, increasing its hyd
295 s of PGA2 by activating Rap1/Rac1 GTPase and protein kinase A targets at cell adhesions and cytoskele
297 of a local pool of cAMP and activation of a protein kinase A type II subset, leading to phosphorylat
299 ially PAK-dependent and likely also involves protein kinase A, which is known to reduce PREX1 functio
300 affected either by blocking the activity of protein kinase A with H89, or by blocking the activity o
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