Ignet

Gene Information

Gene symbol: PDE4A

Gene name: phosphodiesterase 4A, cAMP-specific

HGNC ID: 8780

Related Genes

#	Gene Symbol	Number of hits
1	AKT2	1 hits
2	AVP	1 hits
3	CD36	1 hits
4	INS	1 hits
5	MAPK1	1 hits
6	MAPK14	1 hits
7	NSF	1 hits
8	PDE10A	1 hits
9	PDE1C	1 hits
10	PDE3A	1 hits
11	PDE3B	1 hits
12	PDE4B	1 hits
13	PDE5A	1 hits
14	PDE8B	1 hits
15	PRKAR1A	1 hits
16	PRKAR2A	1 hits
17	SCD	1 hits
18	SUCLG1	1 hits
19	VAMP2	1 hits
20	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	9648839	Cyclic nucleotide phosphodiesterase 3 expression in vivo: evidence for tissue-specific expression of phosphodiesterase 3A or 3B mRNA and activity in the aorta and adipose tissue of atherosclerosis-prone insulin-resistant rats.
2	9648839	With a view of understanding the potential roles of phosphodiesterase (PDE)3 in the acceleration of atherosclerosis in diabetes, we have analyzed the in vivo levels of low Km cAMP PDE3 and PDE4 activities as well as PDE3A and PDE3B mRNA in a relevant animal model.
3	9648839	Thus, in the aorta of atherosclerosis-prone insulin-resistant cp/cp rats, PDE3A gene expression is upregulated, resulting in significantly higher PDE3 activity.
4	9648839	Furthermore, determination of PDE3 activity and PDE3A and PDE3B mRNA levels in heart and white and brown fat tissues of JCR:LA-cp rats revealed that PDE3B mRNA and activity in white adipose tissue is downregulated in this diabetic animal model, and that PDE3A and PDE3B genes are tissue-specifically expressed and differentially regulated in aorta and adipose tissue, respectively, under hyperinsulinemic conditions.
5	9893113	Investigations of recent years revealed that isozymes of cyclic-3', 5'-nucleotide phosphodiesterase (PDE) are a critically important component of the cyclic-3',5'-adenosine monophosphate (cAMP) protein kinase A (PKA) signaling pathway.
6	9893113	Anomalously high PDE4 activity in collecting ducts is a basis of unresponsiveness to vasopressin in mice with hereditary nephrogenic diabetes insipidus.
7	12107047	Marked adaptation to elevated cAMP levels occurred, leading to an increase in total cAMP-specific phosphodiesterase activity, a 50% decline in cAMP-dependent protein kinase (protein kinase A) activity, and an increased expression of G(alpha)(i2).
8	12107047	These data demonstrate the existence of adaptive responses of protein kinase A, phosphodiesterase, and G(alpha)(i2) in tissues expressing constitutively active G(alpha)(s) that may act to rectify the impact of increased cAMP accumulation.
9	12888882	VEGF-induced HUVEC migration and proliferation are decreased by PDE2 and PDE4 inhibitors.
10	12888882	Here, we report that: 1) PDE2, PDE3, PDE4 and PDE5 are expressed in HUVEC; 2) EHNA (20 microM), PDE2 selective inhibitor, and RP73401 (10 microM), PDE4 selective inhibitor, are able to increase the intracellular cAMP level in HUVEC; 3) EHNA and RP73401 are able to inhibit proliferation, cell cycle progression and migration of HUVEC stimulated by VEGF; 4) these in vitro effects can be mimic by treating HUVEC with the cAMP analogue, 8-Br-cAMP (600 microM); 5) only the association of EHNA and RP73401 inhibits in vivo angiogenesis, indicating that both migration and proliferation must be inhibited.
11	12888882	VEGF-induced HUVEC migration and proliferation are decreased by PDE2 and PDE4 inhibitors.
12	12888882	Here, we report that: 1) PDE2, PDE3, PDE4 and PDE5 are expressed in HUVEC; 2) EHNA (20 microM), PDE2 selective inhibitor, and RP73401 (10 microM), PDE4 selective inhibitor, are able to increase the intracellular cAMP level in HUVEC; 3) EHNA and RP73401 are able to inhibit proliferation, cell cycle progression and migration of HUVEC stimulated by VEGF; 4) these in vitro effects can be mimic by treating HUVEC with the cAMP analogue, 8-Br-cAMP (600 microM); 5) only the association of EHNA and RP73401 inhibits in vivo angiogenesis, indicating that both migration and proliferation must be inhibited.
13	12904862	Several studies have shown pancreatic islets or beta cells to contain PDE1C, PDE3B and PDE4, with some evidence for PDE10A.
14	12904862	In contrast, activation of beta-cell PDE3B could mediate the inhibitory effect of IGF-1 and leptin on insulin secretion.
15	15546994	To dissect and quantitate these two separate effects, we compared the skeletal muscle gene-expression profiles of muscle insulin receptor knockout (MIRKO) mice and their Lox controls in the basal, streptozotocin-induced diabetic, and insulin-treated diabetic states.
16	15546994	Pure deficiency of insulin action as present in the MIRKO mouse results in regulation of 130 genes, with down-regulation of NSF (N-ethylmaleimide-sensitive fusion protein) and VAMP-2 (vesicle-associated membrane protein 2), stearoyl CoA desaturase 1, and cAMP-specific phosphodiesterase 4B, as well as up-regulation of some signaling-related genes, such as Akt2, and the fatty-acid transporter CD36.
17	16424109	Unlike insulin, the PI3-K inhibitor wortmannin did not reverse GE antilipolysis, and GE did not affect phosphorylation of protein kinase B (PKB).
18	16424109	The specific phosphodiesterase 4 (PDE4) inhibitor rolipram did not significantly affect insulin antilipolysis, but almost completely reversed GE antilipolysis.
19	17198676	Phosphodiesterase 3B (PDE3B), is known to play an important role in acute insulin and cAMP-mediated regulation of lipid metabolism, and PDE4 are the main PDE types expressed in adipocytes.
20	17198676	Long-term treatment of 3T3-L1 adipocytes with insulin induced up-regulation of PDE3B and PDE4D in a phosphatidylinositol 3-kinase-dependent manner whereas long-term treatment with beta-adrenergic agonists induced down-regulation of PDE3B and up-regulation of PDE4D.
21	17198676	Thus, PDE3B and PDE4D can be added to the list of genes regulated by insulin and cAMP-increasing hormones.
22	17198676	Altered expression of PDE3B and PDE4D in response to long-term treatment with insulin and catecholamines may contribute to altered regulation of metabolism in diabetes.
23	17991719	Diminished phosphodiesterase-8B potentiates biphasic insulin response to glucose.
24	17991719	Using RT-PCR and Western blot analyses, we identified PDE3A, PDE3B, PDE4B, PDE4D, and PDE8B in rat islets and in INS-1E cells and several possible splice variants of these PDEs.
25	17991719	Specific depletion of PDE3A with small interfering (si) RNA (siPDE3A) led to a small (67%) increase in the insulin response to glucose in INS-1E cells but not rat islets. siPDE3A had no effect on the glucagon-like peptide-1 (10 nmol/liter) potentiated insulin response in rat islets.
26	17991719	Depletion in PDE8B levels in rat islets using similar technology (siPDE8B) increased insulin response to glucose by 70%, the potentiation being of similar magnitude during the first and second phase insulin release.
27	17991719	The siPDE8B-potentiated insulin response was further increased by 23% when glucagon-like peptide-1 was included during the glucose stimulus.
28	17991719	We propose that PDE8B, an 3-isobutyl-1-methylxanthine-insensitive cAMP-specific phosphodiesterase, could prove a novel target for enhanced insulin response, affecting a specific pool of cAMP involved in the control of insulin granule trafficking and exocytosis.
29	23251728	Alternatively, treatment targeted towards comorbid organs may alter features of pulmonary disease as statins, angiotensin-converting enzyme (ACE) inhibitors and peroxisome proliferator-activated receptor (PPAR) agonists may have beneficial effects on COPD by reducing exacerbations and mortality.
30	23251728	Newer anti-inflammatory treatments, such as phosphodiesterase 4 (PDE4), nuclear factor(NF)-kB, and p38 mitogen-activated protein kinase (MAPK) inhibitors, are given systemically and may confer benefits to both COPD and its comorbidities.