ライフサイエンスコーパス: PDE2

1 vels because of the allosteric activation of PDE2.

2 produces a second cytoplasmic DHH/DHHA1 PDE Pde2.

3 The adenosine A2A receptor and PDE2, 3, 4, and 7 are important for activity.

4 we examined the role of phosphodiesterase 2 (PDE2), a medium spiny neuron-enriched and cGMP-activated

5 The cross-regulation of PDE1 and PDE2 activities results in counterintuitive control of s

6 In diseased cardiomyocytes, higher PDE2 activity could be further enhanced by stimulation o

7 ras2 and cyr1, as well as elevated dosage of PDE2, allowed cox2::arg8m-G66S to support Arg prototroph

8 PDE2 and GC-D are both expressed in olfactory cilia wher

9 and that it interacts with phosphodiesterase Pde2 and monomeric GTPase Ras1.

10 In PDE2 and PDE5, the GAF domains mediate cGMP stimulation;

11 sequence alignments with the GAF domains of PDE2 and PDE5.

12 press the cGMP-stimulated phosphodiesterase (PDE2) and guanylyl cyclase-D (GC-D), suggesting that cGM

13 h selectivity of >2000-fold over PDE7, PDE9, PDE2, and PDE5.

14 h behavioral data showing that both PDE4 and PDE2 are involved in NMDA receptor-mediated memory proce

15 In PDE2 binding of cGMP to the GAF domain causes an activat

16 eproduction and plant infection, deletion of PDE2 but not PDE1 activated intracellular PKA activities

17 Additionally, Pde2, but not Pde1, degraded pApA into AMP.

18 Increased expression of PDE2 can mediate hyperpermeability effects of paracrine

19 to phosphoadenylyl adenosine (pApA), whereas Pde2 directly hydrolyzed c-di-AMP into AMP.

20 pde2 mutant failed to produce DON, the tri10 pde2 double mutant produced a significantly higher level

21 PDE2 emerges as a novel key regulator of cardiac hypertr

22 n strains lacking the cAMP phosphodiesterase PDE2, even in the absence of nitrogen starvation.

23 Myocardial PDE2 expression and activity were ~2-fold higher in adva

24 via catecholamine infusions in rats enhanced PDE2 expression ~2-fold and cAMP hydrolytic activity ~4-

25 high affinity suggests that cGMP binding to PDE2 GAF-B activates the enzyme rapidly, stoichiometrica

26 phodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and n

27 actory glomeruli" and the phosphodiesterase (PDE2)(+) glomeruli are a subset(s) of the MAb213(+) glom

28 he two cAMP phosphodiesterase genes PDE1 and PDE2 had overlapping functions in vegetative growth, con

29 Among the PDE superfamily, PDE2 has the unique property of being able to be stimula

30 h-affinity cAMP phosphodiesterase encoded by PDE2, have real potential as targets for antifungal chem

31 tent than the natural product CC-1065 (MeCPI-PDE2, IC50 = 7 vs 20 pM).

32 stimulated by exogenous cAMP or deletion of PDE2 in both tri10 and tri6 mutants.

33 se transcription is altered upon deletion of PDE2 in C. albicans has also allowed us to predict that

34 However, the role of PDE2 in HF is poorly understood.

35 denafil) are licensed for PH, but a role for PDE2 in lung physiology and disease has yet to be establ

36 figuration when compared to the structure of PDE2 in the apo state.

37 PDE2 inhibition elicits pulmonary dilation, prevents pul

38 onstrate that the antihypertrophic effect of PDE2 inhibition involves the generation of a local pool

39 ertrophy, whereas increasing cAMP levels via PDE2 inhibition is antihypertrophic.

40 Herein, we investigated whether PDE2 inhibition modulates pulmonary cyclic nucleotide si

41 is via nitric oxide donors, whereas specific PDE2 inhibition partially restored beta-AR responsivenes

42 PDE2 inhibition represents a viable, orally active thera

43 The selective PDE2 inhibitor BAY 60-7550 augmented atrial natriuretic

44 present study investigated how the selective PDE2 inhibitor BAY60-7550 (BAY) affected Abeta-induced l

45 activity was inhibited by EHNA, a selective PDE2 inhibitor, and was stimulated three-fold by cGMP.

46 dependent PDE responses, but not 2 different PDE2 inhibitors.

47 Phosphodiesterase 2 (PDE2) inhibitors increase the intracellular cAMP and/or

48 dorant signaling is initiated; however, only PDE2 is expressed in axons.

49 PDE2 is markedly up-regulated in failing hearts and dese

50 Previously, we have shown that PDE2 is required for hyphal development and cell wall in

51 TRI gene-expression and DON production, and Pde2 is the major cAMP phosphodiesterase to negatively r

52 ated whether myocardial phosphodiesterase-2 (PDE2) is altered in heart failure (HF) and determined PD

53 (cGMP) stimulated human phosphodiesterase 2 (PDE2) is expressed mainly in brain and heart tissues.

54 Thus, activating myocardial PDE2 may represent a novel intracellular antiadrenergic

55 However, it remains unclear whether PDE2 mediated neuroapoptotic and neuroinflammatory event

56 altered in heart failure (HF) and determined PDE2-mediated effects on beta-adrenergic receptor (beta-

57 PDE2 mediates ANP/cGMP-induced decreases in aldosterone

58 ance energy transfer biosensor revealed that PDE2 mediates NP/cGMP-driven decreases of submembrane cA

59 Whereas the tri6 pde2 mutant failed to produce DON, the tri10 pde2 double

60 Using a pde2 mutant strain, pApA was detected for the first time

61 Overexpression of PDE2 or deletion of RAS2 rescued the temperature sensiti

62 lipolysis was altered by inhibition of PDE1, PDE2, or PDE8A.

63 Importantly, PDE2-overexpressing cardiomyocytes showed marked protect

64 Accordingly, PDE2 overexpression in healthy cardiomyocytes reduced th

65 i), and multiple phosphodiesterase isoforms (PDE2, PDE3, and PDE4).

66 tial homology to the cGMP-binding domains of PDE2, PDE5 and PDE6 as well as a carboxy-terminal region

67 ogous to many signaling molecules, including PDE2, PDE5, and PDE6, which likely constitute a low-affi

68 tory regions found in the cGMP-binding PDEs: PDE2, PDE5, and PDE6.

69 results also demonstrated that both Pde1 and Pde2 played roles in bacterial growth, resistance to UV

70 Although capable of hydrolyzing c-di-AMP, Pde2 preferentially converts linear 5'-phosphadenylyl-ad

71 in SA (DSA-TMI, IC50 = 5 vs 8 pM), and MeCTI-PDE2 proved to be 3-fold more potent than the natural pr

72 Pde2 remains functionally dispensable, but Ras1 is found

73 cGMP are selectively hydrolyzed by PDE4 and PDE2, respectively, in rat primary cerebral cortical and

74 We found that inhibiting PDE2 resulted in enhancement of dopamine-induced surface

75 actor-alpha-induced endothelial NP/GC-A/cGMP/PDE2 signaling impairs endothelial barrier functions.

76 own to directly regulate steroidogenesis was PDE2, the cGMP-stimulated PDE.

77 the atrial natriuretic peptide (ANP), making PDE2-type enzymes important targets for drug discovery.

78 Neither Pde1 nor Pde2 was necessary for the repression of hyphal growth b

79 Both SPD_2032 (Pde1) and SPD_1153 (Pde2), which belong to the DHH subfamily 1 proteins, dis

80 vior of the ubp3Delta mutant, overexpressing PDE2, which encodes a phosphodiesterase that hydrolyzes