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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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