Cyclic nucleotide phosphodiesterases: Relating structure and function

Sh, Francis; Turko,; Jd, Corbin

doi:10.1016/s0079-6603(00)65001-8

Cited by 515 publications

(481 citation statements)

References 273 publications

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“…Another component that contributes to complex and differential cAMP signaling, in addition to the presence of different cAMP effectors, is the phosphodiesterases which are differentially expressed in different cells [7,8]. Our results indicate that PDE3B and PDE4 control cAMP pools which negatively influence PKB phosphorylation induced primarily by insulin but to certain extent also by CL16243.…”

Section: Discussionmentioning

confidence: 73%

“…Highly conserved PDEs are tissue specific and differentially distributed in cells and cellular compartments. They form a large group of enzymes consisting of eleven families (PDE1-11), characterized by different substrate affinities, biochemical and physical properties, different mechanisms whereby they are regulated, and different sensitivities to inhibitors [6,7]. Adipocytes express mainly PDE3B and PDE4s.…”

Section: Introductionmentioning

confidence: 99%

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Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4

Zmuda-Trzebiatowska

Manganiello

Degerman

2007

Cellular Signalling

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Crosstalk between insulin and cAMP signalling pathways has a great impact on adipocyte metabolism. Whilst Protein kinase B (PKB) is a pivotal mediator of insulin action, in some cells regulation of PKB by cAMP has also been demonstrated. Here we provide evidence that, in a phosphatidyl inositol 3-kinase dependent manner, β3-adrenergic stimulation (using CL316243) in adipocytes induces PKB phosphorylation in the absence of insulin and also potentiates insulin-induced phosphorylation of PKB. Interestingly, insulin-and CL316243-induced PKB phosphorylation was found to be inhibited by pools of cAMP controlled by PDE3B and PDE4 (mainly in the context of insulin), whereas a cAMP pool controlling protein kinase A appeared to mediate stimulation of PKB phosphorylation (mainly in the context of CL316243).

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Section: Discussionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4

Zmuda-Trzebiatowska

Manganiello

Degerman

2007

Cellular Signalling

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“…Several isoforms of PDE are known to exist (Francis, Turko et al 2001). PDE4 is a cAMP-specific PDE that is prevalent in the brain and is the target of antidepressant and cognitive enhancing pharmacotherapeutics.…”

Section: Cyclic Amp Cascadementioning

confidence: 99%

The cyclic AMP phenotype of fragile X and autism

Kelley

Bhattacharyya

Lahvis

et al. 2008

Neuroscience & Biobehavioral Reviews

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Cyclic AMP (cAMP) is a second messenger involved in many processes including mnemonic processing and anxiety. Memory deficits and anxiety are noted in the phenotype of fragile X (FX), the most common heritable cause of mental retardation and autism. Here we review reported observations of altered cAMP cascade function in FX and autism. Cyclic AMP is a potentially useful biochemical marker to distinguish autism comorbid with FX from autism per se and the cAMP cascade may be a viable therapeutic target for both FX and autism.

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“…Eleven PDE families (PDE1-11) have been identified based on their substrate affinities, biochemical and physical properties, mechanisms whereby they are regulated and different sensitivities to inhibitors [1,2]. Adipocytes express membrane-bound PDE3B and membrane bound as well as cytosolic PDE4s [3].…”

Section: Introductionmentioning

confidence: 99%

Long-term regulation of cyclic nucleotide phosphodiesterase type 3B and 4 in 3T3-L1 adipocytes

Oknianska¹,

Zmuda-Trzebiatowska²,

Manganiello³

et al. 2007

Biochemical and Biophysical Research Communications

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Phosphodiesterase 3B (PDE3B), 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. Here we show that members of all PDE4 isoforms are expressed in 3T3-L1 and primary mouse adipocytes. 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 β-adrenergic agonists induced down-regulation of PDE3B and up-regulation of PDE4D. Thus, PDE3B and PDE4D can be added to the list of genes regulated by insulin and cAMP-increasing hormones. 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.

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Cyclic nucleotide phosphodiesterases: Relating structure and function

Cited by 515 publications

References 273 publications

Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4

Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4

The cyclic AMP phenotype of fragile X and autism

Long-term regulation of cyclic nucleotide phosphodiesterase type 3B and 4 in 3T3-L1 adipocytes

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