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1 ity of cAMP-hydrolyzing phosphodiesterase 3 (PDE3).
2 ulated by inhibition of phosphodiesterase 3 (PDE3).
3  efficient membrane association/targeting of PDE3.
4 and PDE4, but not IL-4-induced activation of PDE3.
5 inone and cilostazol, specific inhibitors of PDE3.
6  secretion, its action may be independent of PDE3.
7  and increased intracellular cAMP levels via PDE3/4 inhibition and subsequent stimulation of the PKA-
8                                     Combined PDE3/4 inhibition did not induce T cell apoptosis, sugge
9 ognised that the use of PDE3, PDE4 and mixed PDE3/4 inhibitors can provide clinical benefit to patien
10 ced in Pkd2(-/WS25);Pde3a(-/-) mice, despite PDE3 accounting for only a small fraction of renal cAMP
11 on; another cAMP pool that is metabolized by PDE3 activates another PKA (isozyme or pool) which suppr
12 s can be designed with flexible size against PDE3 active site.
13            In contrast, higher total PDE and PDE3 activities in adult IDC patients treated with PDE3i
14  4D, a cGMP-specific PDE, and of particulate PDE3, activities in betaTC3 insulinoma cells.
15 E3A protein levels correlated with decreased PDE3 activity and increased cAMP levels in EC.
16                Furthermore, determination of PDE3 activity and PDE3A and PDE3B mRNA levels in heart a
17 lic and microsomal membrane protein for cAMP PDE3 activity assays.
18 istent with our hypothesis that an increased PDE3 activity in aortic smooth muscle cells may contribu
19                                    Moreover, PDE3 activity is required for insulin/insulin-like growt
20                                 We find that PDE3 activity is the major low Km cAMP activity in the a
21    Little is known about relative changes in PDE3 activity or gene expression during the evolution of
22  chromatography of solubilized SR membranes, PDE3 activity was recovered in distinct high molecular w
23          Consistent with these observations, PDE3 activity was reduced approximately 8-fold in SR fra
24 regulated, resulting in significantly higher PDE3 activity.
25 tion (P<.05) in microsomal but not cytosolic PDE3 activity.
26 tion of PKA via cGMP-dependent inhibition of PDE3 activity.
27 we found that it required a combination of a PDE3 and a PDE4 inhibitor to fully induce UCP1 mRNA and
28 olysis in microsomal fractions by inhibiting PDE3 and in cytosolic fractions by inhibiting both PDE3
29 p with a methoxy group raised the IC(50) for PDE3 and PDE1, yet only slightly changed the IC(50) for
30 nd in cytosolic fractions by inhibiting both PDE3 and PDE1.
31 or PDE4, but actually lowered the IC(50) for PDE3 and PDE1.
32 e analyzed the in vivo levels of low Km cAMP PDE3 and PDE4 activities as well as PDE3A and PDE3B mRNA
33 lase activities, and stimulate cAMP-specific PDE3 and PDE4 and cGMP-specific PDE5 activities.
34 in (PI3-K inhibitor) inhibited activation of PDE3 and PDE4 by IL-4.
35                          We report here that PDE3 and PDE4 expression levels are lower in human ADPKD
36                         However, the role of PDE3 and PDE4 in the regulation of cardiomyocyte apoptos
37 he rise in cAMP resulting from inhibition of PDE3 and PDE4 induces hypertrophy, whereas increasing cA
38            This effect was magnified by dual PDE3 and PDE4 inhibition.
39 hese data provide a rationale for the use of PDE3 and PDE4 inhibitors in the treatment of COPD and as
40 tors alone had no effect, the combination of PDE3 and PDE4 inhibitors induced ATF-1/CREB serine 63/13
41  when injected into mice, the combination of PDE3 and PDE4 inhibitors stimulated glucose uptake in BA
42 he coincident signaling of the major cardiac PDE3 and PDE4 isoforms, thus orchestrating a feedback lo
43 firmed by in situ hybridization studies with PDE3 and PDE4 probes.
44 ts suggested that IL-4-induced activation of PDE3 and PDE4 was downstream of IRS-2/PI3-K, not STAT6,
45   Mammalian phosphodiesterase types 3 and 4 (PDE3 and PDE4) hydrolyze cAMP and are essential for the
46  Mammalian phosphodiesterases types 3 and 4 (PDE3 and PDE4) hydrolyze cAMP and are essential for the
47 erent TCC contained different proportions of PDE3 and PDE4, and their activities increased during Ag
48 drolyzing phosphodiesterases (PDEs), such as PDE3 and PDE4, coexist in cardiomyocytes and elicit diff
49 ant MBP epitope (amino acids 83-99), contain PDE3 and PDE4, two PDEs that exhibit a high affinity for
50 tivated cyclic nucleotide phosphodiesterases PDE3 and PDE4, whereas IL-3, granulocyte-macrophage CSF
51  basal PDE activity was mainly restricted to PDE3 and PDE5 activity.
52 of a novel inhaled dual phosphodiesterase 3 (PDE3) and PDE4 inhibitor, RPL554 for its ability to act
53 ce regulator (CFTR) -driven fluid secretion (PDE3), and response to vasopressin V2 receptor activatio
54 d multiple phosphodiesterase isoforms (PDE2, PDE3, and PDE4).
55 hostins were also potent inhibitors of PDE1, PDE3, and PDE4.
56  a methoxy group raised the IC(50) for PDE1, PDE3, and PDE4.
57                   Importantly, inhibition of PDE3, and thus perturbation of the spatiotemporal regula
58 A activity and identify phosphodiesterase 3 (PDE3) as a critical regulator in maintaining this spatia
59 creatic islets, inhibition of both PDE1C and PDE3 augmented glucose-dependent insulin secretion.
60 ibited cAMP-hydrolyzing phosphodiesterase 3 (PDE3) blocked SNAP- and CNP-elicited effects on NF-kappa
61 ltured cardiomyocytes, chronic inhibition of PDE3 but not PDE4 activity by pharmacological agents or
62 structure increased the potency for PDE1 and PDE3, but not PDE4.
63 F) or PKC (PMA), but selective activation of PDE3 by IL-4 is MAP kinase independent (but perhaps IRS-
64                    The N-terminal portion of PDE3 can be arbitrarily divided into region 1 (aa 1-300)
65 ial and harmful effects, and, if so, whether PDE3 can be targeted so as to increase contractility wit
66 ve inhibition of PDE4, but not inhibition of PDE3, causes a time- and dose-dependent accumulation of
67                            Three isoforms of PDE3 (cGMP-inhibited) cyclic nucleotide phosphodiesteras
68                                     Specific PDE3 (cilostamide) and PDE4 (rolipram) inhibitors suppre
69 ut not by specific inhibitors of the PDE1 or PDE3 classes.
70 ic activity in microsomal fractions, whereas PDE3 constitutes the majority of cAMP hydrolytic activit
71 ounts of N-terminal sequence, aggregation of PDE3 decreased, and H3A-Delta607, H3A-Delta721, and M3B-
72 cellular compartments of human myocardium by PDE3-dependent and PDE3-independent mechanisms.
73 trophy after transverse aortic constriction, PDE3 effects were not affected, whereas the contribution
74 transcription polymerase chain reaction, and PDE3 enzyme activity by cAMP-hydrolysis.
75 tation, PDE3A1 mRNA abundance and microsomal PDE3 enzyme activity were increased by 1.7-fold to 1.8-f
76                               In particular, PDE3 enzymes play a major role in regulating cAMP metabo
77 ents with heart failure, the contribution of PDE3 expression/activity in heart failure is not well kn
78                                          The PDE3 family comprises two highly homologous subtypes exp
79                                  A number of PDE3 family selective inhibitors have been approved by t
80  ICa-L after the cGMP-inhibited PDE isozyme (PDE3) had been selectively inhibited by milrinone (5 mum
81 lectively activates PKG but does not inhibit PDE3, had no effect on NF-kappaB-mediated transcription.
82 resented by compound 4c: PDE1, IC50 = 60 nM; PDE3, IC50 = 55,000 nM; PDE5, IC50 = 75 nM.
83 e supported a switching from cGMP acting via PDE3 in control neurons to PDE2A in SHR neurons in the m
84 ts of human myocardium by PDE3-dependent and PDE3-independent mechanisms.
85 and SERCA2 activity; this was potentiated by PDE3 inhibition but not by PDE4 inhibition.
86                                 Furthermore, PDE3 inhibition had no effect on PDE3A(-/-) hearts but i
87 ations in the heart rather than nonselective PDE3 inhibition is cardioprotective in the long term.
88 ments of human myocardium and the effects of PDE3 inhibition on cAMP hydrolysis in these compartments
89  very useful tool to evaluate the effects of PDE3 inhibition on lipolysis and metabolic rate and migh
90                  These results indicate that PDE3 inhibition regulates endothelial CD39 at a post-tra
91 39 mRNA and protein were both elevated after PDE3 inhibition.
92 l was displaced to the left by PDE4, but not PDE3, inhibition.
93 enoceptor stimulation of brown adipocytes, a PDE3 inhibitor alone could potentiate induction of UCP1
94 e apoptotic protein BAD was inhibited by the PDE3 inhibitor cilostamide.
95                                          The PDE3 inhibitor, cilostamide, showed especially strong cG
96  to -5 inhibitors revealed that the specific PDE3 inhibitor, milrinone, accelerated spontaneous firin
97 ipram, but not the cAMP phosphodiesterase-3 (PDE3) inhibitor cilostamide, causes profound growth arre
98 und that cilostamide, a phosphodiesterase 3 (PDE3) inhibitor, (i) reversed the established effects of
99                                              PDE3 inhibitors (PDE3i) are used for short-term treatmen
100                                      Whereas PDE3 inhibitors alone had no effect, the combination of
101                                      ISO and PDE3 inhibitors also induced the PDE3A-ICER feedback loo
102 es cAMP-mediated signaling in the heart, and PDE3 inhibitors augment contractility in patients with h
103               Molecular models show that the PDE3 inhibitors cilostazol and milrinone share some of c
104 thelial cells (HUVECs) were treated with the PDE3 inhibitors cilostazol and milrinone, then analyzed
105                  The combination of PDE4 and PDE3 inhibitors expresses synergistic effects and may br
106                                              PDE3 inhibitors have been used to 'overcome' the reducti
107              Although chronic treatment with PDE3 inhibitors increases mortality in patients with hea
108 chniques we analyzed the effects of PDE4 and PDE3 inhibitors on human immune cells to address these d
109 lls and was inhibited to a greater extent by PDE3 inhibitors than by rolipram, a PDE4 inhibitor.
110                                              PDE3 inhibitors, by raising cAMP content, have acute ino
111  of PDE4, rolipram and denbufylline, whereas PDE3 inhibitors, cilostamide and lixazinone, had no effe
112  in patients with heart failure treated with PDE3 inhibitors.
113                       Phosphodiesterase III (PDE3) inhibitors are inotropic agents used to treat cong
114                                   Therefore, PDE3 is a novel mediator of inflammation in VSMCs.
115 yte and that regulation of the activity of a PDE3 is a step distal to the kinase activation.
116 se <4.5 mmol); the crosstalk between AKT and PDE3 is responsible for efficient catabolic response und
117       Cyclic nucleotide phosphodiesterase 3 (PDE3) is an important regulator of cyclic adenosine mono
118 e findings indicate that the contribution of PDE3 isoforms to the regulation of cAMP hydrolysis in in
119 ort the conclusion that PDE3A is the primary PDE3 isozyme modulating basal contractility and SR Ca(2+
120 KD, we examined cyst development in Pde1- or Pde3-knockout mice on the Pkd2(-/WS25) background (WS25
121 Xenopus oocytes and rescues the phenotype of pde3(-/-) mouse oocytes.
122 reverse transcription-PCR indicated that TCC PDE3 mRNA was of the PDE3B, not PDE3A, subtype.
123 seases, It is now recognised that the use of PDE3, PDE4 and mixed PDE3/4 inhibitors can provide clini
124 +)/calmodulin-activated (PDE1) and other non-PDE3 phosphodiesterases reduces their contribution to <2
125 n the dual cAMP/cGMP binding capabilities of PDE3, provide the molecular basis for inhibitor specific
126      Cyclic nucleotide phosphodiesterase 3A (PDE3) regulates cAMP-mediated signaling in the heart, an
127                                Inhibition of PDE3 results in increased HDAC-1 phosphorylation, leadin
128 lex with a generic PDE inhibitor and a novel PDE3 selective inhibitor.
129  3-isobutyl-1-methylxanthine (IBMX), and the PDE3 selective inhibitors milrinone and cilostazol each
130  To identify amino acid residues involved in PDE3-selective inhibitor binding, we selected eight pres
131 h these results, inhibitors of PDE4, but not PDE3, selectively abolished the lateral confinement of c
132  cAMP-dependent transcription, inhibitors of PDE3 (siguazodan, cilostazol) and PDE4 (rolipram, GSK256
133 pecific (74.6+/-13.8 pmol/mg per minute) and PDE3-specific (48.2+/-15.9 pmol/mg per minute) activitie
134                  In addition, total PDE- and PDE3-specific activities were not altered in pediatric I
135 r specific for the type 3 phosphodiesterase (PDE3), suggesting that the activity of a PDE is required
136 tion, after natriuretic peptide stimulation, PDE3 was also involved in cGMP/cAMP crosstalk.
137 Ca,L)) by approximately 46%, indicating that PDE3 was the major constitutively active PDE in the basa
138 vely activated MEK, MAP kinase and PDE4, not PDE3, were activated.
139 tes mitogenesis is determined by activity of PDE3, whereas another cAMP-PKA pathway is directed by ac
140 ctive or only weakly active as inhibitors of PDE3, which is a major isozyme involved in cAMP hydrolys
141 al determinants important for association of PDE3 with intracellular membranes, as well for self-asso

 
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