ライフサイエンスコーパス: PDE1

1 osolic fractions by inhibiting both PDE3 and PDE1.

2 but actually lowered the IC(50) for PDE3 and PDE1.

3 electivity in inhibiting other PDE isozymes (PDE1-4 and PDE6) were evaluated.

4 itor, sildenafil, but it is inhibited by the PDE1/5 inhibitor (+)-cis-5,6a, 7,8,9 hyl] phenylmethyl]-

5 nd plant infection, deletion of PDE2 but not PDE1 activated intracellular PKA activities and increase

6 METHODS AND Inhibition of PDE1 activity using a PDE1-selective inhibitor, IC86340,

7 heral blood lymphocytes (HPBL) are devoid of PDE1 activity.

8 The cross-regulation of PDE1 and PDE2 activities results in counterintuitive con

9 lthough the two cAMP phosphodiesterase genes PDE1 and PDE2 had overlapping functions in vegetative gr

10 Our results also demonstrated that both Pde1 and Pde2 played roles in bacterial growth, resistan

11 rphostin structure increased the potency for PDE1 and PDE3, but not PDE4.

12 t combination of potency and selectivity for PDE1 and PDE5 cGMP PDEs as represented by compound 4c: P

13 e inhibitors of the cGMP-hydrolyzing enzymes PDE1 and PDE5.

14 bitors with IC50 values below 30 nM for both PDE1 and PDE5.

15 an sildenafil with better selectivity toward PDE1 and PDE6.

16 terase (PDE): Ca2+-calmodulin dependent PDE (PDE1) and cAMP-specific PDE (PDE4).

17 , activation of Ca(2+)/calmodulin-activated (PDE1) and other non-PDE3 phosphodiesterases reduces thei

18 Both SPD_2032 (Pde1) and SPD_1153 (Pde2), which belong to the DHH subfa

19 secretion by ADPKD cells than inhibition of PDE1, and inhibition of PDE4 induced cyst-like dilations

20 In contrast, inhibition of PDE1 caused greater stimulation of extracellular signal-

21 Pde1 cleaved c-di-AMP into phosphoadenylyl adenosine (pA

22 PDE1 coimmunoprecipitated with B-Raf and A-kinase anchor

23 een calcium and cyclic nucleotide signaling (PDE1), control of cell proliferation and cystic fibrosis

24 The findings here extend the PDE1 data to the dog and contribute to our understanding

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

26 s than inhibition of PDE4, and inhibition of PDE1 enhanced AVP-induced ERK activation.

27 We have characterized a completely purified PDE1 enzyme from dog heart using dye-affinity, Mono-Q an

28 c (PDE4) and the Ca2+/calmodulin-stimulated (PDE1) families were found to predominate in assays using

29 /calmodulin (CaM)-activated cGMP-hydrolyzing PDE1 family may play a pivotal role in balancing intrace

30 Isoforms in the PDE1 family of cyclic nucleotide phosphodiesterases were

31 DE5 cGMP PDEs as represented by compound 4c: PDE1, IC50 = 60 nM; PDE3, IC50 = 55,000 nM; PDE5, IC50 =

32 nvestigate the role of Ca(2+)/CaM-stimulated PDE1 in regulating pathological cardiomyocyte hypertroph

33 gested the presence of an additional form of PDE1, in heart only, separate from the PDE1A group which

34 In cultured SMCs, PDE1C deficiency or PDE1 inhibition attenuated SMC proliferation and migrati

35 PDE1 inhibition can increase cAMP and cGMP levels, activ

36 nificantly attenuated by PDE1C deficiency or PDE1 inhibition in vivo.

37 PDE1 inhibition suppressed vascular remodeling of human

38 Importantly, administration of the PDE1 inhibitor IC86340 attenuated cardiac hypertrophy in

39 erosis using antisense oligonucleotides or a PDE1 inhibitor results in suppression of SMC proliferati

40 are treated with a phosphodiesterase type 1 (PDE1) inhibitor during the period of monocular deprivati

41 s of potent thienotriazolopyrimidinone-based PDE1 inhibitors was discovered.

42 Pde1 is purified by sequential BioRex-70, PBE118, and Mo

43 PDE1 is the only PDE family activated by Ca(2+), which i

44 We examined the expression of PDE1 isoforms in human myocardium, characterized their c

45 hose of normal human kidneys (NHKs), whereas PDE1 levels are not significantly different.

46 Western blotting with isoform-selective anti-PDE1 monoclonal antibodies showed PDE1C1 to be the princ

47 Neither Pde1 nor Pde2 was necessary for the repression of hyphal

48 ipram, but not by specific inhibitors of the PDE1 or PDE3 classes.

49 Inhibition of PDE1 or PDE4 activity by selective inhibitors induced RP

50 esis of PKD, we examined cyst development in Pde1- or Pde3-knockout mice on the Pkd2(-/WS25) backgrou

51 idate a novel role for Ca(2+)/CaM-stimulated PDE1, particularly PDE1A, in regulating pathological car

52 ow that the mRNA encoding the 63-kDa form of PDE1 (PDE1B1) is expressed in RPMI-8392 cells, but not i

53 1 nor lipolysis was altered by inhibition of PDE1, PDE2, or PDE8A.

54 s tyrphostins were also potent inhibitors of PDE1, PDE3, and PDE4.

55 e with a methoxy group raised the IC(50) for PDE1, PDE3, and PDE4.

56 rtial purification of a novel yeast protein, Pde1, present in Apn1-deficient cells.

57 etic approaches, we found that inhibition of PDE1 resulted in a decrease in surface AMPAR levels beca

58 ellular fractions was quantified using a new PDE1-selective inhibitor, IC295.

59 HODS AND Inhibition of PDE1 activity using a PDE1-selective inhibitor, IC86340, or downregulation of

60 PDE1-selective inhibitors were equally effective in inhi

61 The PDE1-specific inhibitor vinpocetine partially restored t

62 obal intracellular cAMP and Cl(-) secretion, PDE1 specifically affects the cAMP signal to the B-Raf/M

63 Notably, inhibition of PDE1, the only family of Ca(2+)-regulated PDEs, also ind

64 A comparison of specific PDE1 to -5 inhibitors revealed that the specific PDE3 in

65 50 of 70 pM, is the most potent inhibitor of PDE1, while 50, with an IC50 of 4 nM, is the most potent

66 methoxy group raised the IC(50) for PDE3 and PDE1, yet only slightly changed the IC(50) for PDE4.