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1 vels because of the allosteric activation of PDE2.
2 nd two putative phosphodiesterases, GdpP and Pde2.
3  produces a second cytoplasmic DHH/DHHA1 PDE Pde2.
4               The adenosine A2A receptor and PDE2, 3, 4, and 7 are important for activity.
5 we examined the role of phosphodiesterase 2 (PDE2), a medium spiny neuron-enriched and cGMP-activated
6             The cross-regulation of PDE1 and PDE2 activities results in counterintuitive control of s
7           In diseased cardiomyocytes, higher PDE2 activity could be further enhanced by stimulation o
8 ras2 and cyr1, as well as elevated dosage of PDE2, allowed cox2::arg8m-G66S to support Arg prototroph
9                                              PDE2 and GC-D are both expressed in olfactory cilia wher
10  of the null mutant of GdpP, suggesting that Pde2 and GdpP play distinctive roles in c-di-AMP signali
11 and that it interacts with phosphodiesterase Pde2 and monomeric GTPase Ras1.
12                                           In PDE2 and PDE5, the GAF domains mediate cGMP stimulation;
13  sequence alignments with the GAF domains of PDE2 and PDE5.
14 press the cGMP-stimulated phosphodiesterase (PDE2) and guanylyl cyclase-D (GC-D), suggesting that cGM
15 h selectivity of >2000-fold over PDE7, PDE9, PDE2, and PDE5.
16 h behavioral data showing that both PDE4 and PDE2 are involved in NMDA receptor-mediated memory proce
17                        Consequently, the CNP-PDE2 axis represents a novel and attractive target for f
18                                           In PDE2 binding of cGMP to the GAF domain causes an activat
19 eproduction and plant infection, deletion of PDE2 but not PDE1 activated intracellular PKA activities
20                                Additionally, Pde2, but not Pde1, degraded pApA into AMP.
21                      Increased expression of PDE2 can mediate hyperpermeability effects of paracrine
22 al PDE2 inhibition or cardiomyocyte-specific PDE2 deletion.
23                             CNP shows strong PDE2-dependent antiarrhythmic effects.
24 to phosphoadenylyl adenosine (pApA), whereas Pde2 directly hydrolyzed c-di-AMP into AMP.
25 pde2 mutant failed to produce DON, the tri10 pde2 double mutant produced a significantly higher level
26                                              PDE2 emerges as a novel key regulator of cardiac hypertr
27 n strains lacking the cAMP phosphodiesterase PDE2, even in the absence of nitrogen starvation.
28                                   Myocardial PDE2 expression and activity were ~2-fold higher in adva
29 via catecholamine infusions in rats enhanced PDE2 expression ~2-fold and cAMP hydrolytic activity ~4-
30  high affinity suggests that cGMP binding to PDE2 GAF-B activates the enzyme rapidly, stoichiometrica
31 phodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and n
32 e locus, we identified a 4-nt variant in the PDE2 gene that occurs in common laboratory strains and s
33 actory glomeruli" and the phosphodiesterase (PDE2)(+) glomeruli are a subset(s) of the MAb213(+) glom
34 he two cAMP phosphodiesterase genes PDE1 and PDE2 had overlapping functions in vegetative growth, con
35                   Among the PDE superfamily, PDE2 has the unique property of being able to be stimula
36 h-affinity cAMP phosphodiesterase encoded by PDE2, have real potential as targets for antifungal chem
37 tent than the natural product CC-1065 (MeCPI-PDE2, IC50 = 7 vs 20 pM).
38  stimulated by exogenous cAMP or deletion of PDE2 in both tri10 and tri6 mutants.
39 se transcription is altered upon deletion of PDE2 in C. albicans has also allowed us to predict that
40                         However, the role of PDE2 in HF is poorly understood.
41 denafil) are licensed for PH, but a role for PDE2 in lung physiology and disease has yet to be establ
42 nol-stimulated L-type Ca(2+) current through PDE2 in mouse and human atrial myocytes.
43 figuration when compared to the structure of PDE2 in the apo state.
44                                              PDE2 inhibition elicits pulmonary dilation, prevents pul
45 onstrate that the antihypertrophic effect of PDE2 inhibition involves the generation of a local pool
46 ertrophy, whereas increasing cAMP levels via PDE2 inhibition is antihypertrophic.
47              Herein, we investigated whether PDE2 inhibition modulates pulmonary cyclic nucleotide si
48  reversed by either specific pharmacological PDE2 inhibition or cardiomyocyte-specific PDE2 deletion.
49 is via nitric oxide donors, whereas specific PDE2 inhibition partially restored beta-AR responsivenes
50  high-dose catecholamine injections in mice, PDE2 inhibition prevented the antiarrhythmic effect of C
51                                              PDE2 inhibition represents a viable, orally active thera
52                                The selective PDE2 inhibitor BAY 60-7550 augmented atrial natriuretic
53 present study investigated how the selective PDE2 inhibitor BAY60-7550 (BAY) affected Abeta-induced l
54  activity was inhibited by EHNA, a selective PDE2 inhibitor, and was stimulated three-fold by cGMP.
55 dependent PDE responses, but not 2 different PDE2 inhibitors.
56                         Phosphodiesterase 2 (PDE2) inhibitors increase the intracellular cAMP and/or
57 dorant signaling is initiated; however, only PDE2 is expressed in axons.
58                                              PDE2 is markedly up-regulated in failing hearts and dese
59               Previously, we have shown that PDE2 is required for hyphal development and cell wall in
60  TRI gene-expression and DON production, and Pde2 is the major cAMP phosphodiesterase to negatively r
61 ated whether myocardial phosphodiesterase-2 (PDE2) is altered in heart failure (HF) and determined PD
62 (cGMP) stimulated human phosphodiesterase 2 (PDE2) is expressed mainly in brain and heart tissues.
63                  Thus, activating myocardial PDE2 may represent a novel intracellular antiadrenergic
64          However, it remains unclear whether PDE2 mediated neuroapoptotic and neuroinflammatory event
65 altered in heart failure (HF) and determined PDE2-mediated effects on beta-adrenergic receptor (beta-
66 hus, CNP might promote beneficial effects of PDE2-mediated negative crosstalk between cAMP and cGMP s
67                                              PDE2 mediates ANP/cGMP-induced decreases in aldosterone
68 ance energy transfer biosensor revealed that PDE2 mediates NP/cGMP-driven decreases of submembrane cA
69                             Whereas the tri6 pde2 mutant failed to produce DON, the tri10 pde2 double
70                                      Using a pde2 mutant strain, pApA was detected for the first time
71                                          The Pde2 null mutant exhibited a lower growth rate and incre
72 l virulence of S. pyogenes, as both DacA and Pde2 null mutants were highly attenuated in a mouse mode
73                            Overexpression of PDE2 or deletion of RAS2 rescued the temperature sensiti
74 lipolysis was altered by inhibition of PDE1, PDE2, or PDE8A.
75                                 Importantly, PDE2-overexpressing cardiomyocytes showed marked protect
76                                 Accordingly, PDE2 overexpression in healthy cardiomyocytes reduced th
77 i), and multiple phosphodiesterase isoforms (PDE2, PDE3, and PDE4).
78 tial homology to the cGMP-binding domains of PDE2, PDE5 and PDE6 as well as a carboxy-terminal region
79 ogous to many signaling molecules, including PDE2, PDE5, and PDE6, which likely constitute a low-affi
80 tory regions found in the cGMP-binding PDEs: PDE2, PDE5, and PDE6.
81                       Atrial cGMP levels and PDE2 (phosphodiesterase 2) activity were reduced in NPR-
82 ntiarrhythmic effects of CNP are mediated by PDE2 (phosphodiesterase 2), which has the unique propert
83 results also demonstrated that both Pde1 and Pde2 played roles in bacterial growth, resistance to UV
84    Although capable of hydrolyzing c-di-AMP, Pde2 preferentially converts linear 5'-phosphadenylyl-ad
85 in SA (DSA-TMI, IC50 = 5 vs 8 pM), and MeCTI-PDE2 proved to be 3-fold more potent than the natural pr
86                                              Pde2 remains functionally dispensable, but Ras1 is found
87  cGMP are selectively hydrolyzed by PDE4 and PDE2, respectively, in rat primary cerebral cortical and
88                     We found that inhibiting PDE2 resulted in enhancement of dopamine-induced surface
89 actor-alpha-induced endothelial NP/GC-A/cGMP/PDE2 signaling impairs endothelial barrier functions.
90 mine antiarrhythmic effects of cGMP-mediated PDE2 stimulation by CNP, we analyzed arrhythmic events a
91 own to directly regulate steroidogenesis was PDE2, the cGMP-stimulated PDE.
92 the atrial natriuretic peptide (ANP), making PDE2-type enzymes important targets for drug discovery.
93                             Neither Pde1 nor Pde2 was necessary for the repression of hyphal growth b
94                                     DacA and Pde2 were critical to the production of the virulence fa
95           Both SPD_2032 (Pde1) and SPD_1153 (Pde2), which belong to the DHH subfamily 1 proteins, dis
96 vior of the ubp3Delta mutant, overexpressing PDE2, which encodes a phosphodiesterase that hydrolyzes