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Phosphodiesterase 4C, cAMP-specific

PDE4C, phosphodiesterase 4C
The protein encoded by this gene belongs to the cyclic nucleotide phosphodiesterase (PDE) family, and PDE4 subfamily. This PDE hydrolyzes the second messenger, cAMP, which is a regulator and mediator of a number of cellular responses to extracellular signals. Thus, by regulating the cellular concentration of cAMP, this protein plays a key role in many important physiological processes. Alternatively spliced transcript variants encoding different isoforms have been described for this gene.[provided by RefSeq, Jul 2011] (from NCBI)
Top mentioned proteins: Phosphodiesterase, PDE4D, PDE4B, PDE, POLYMERASE
Papers on PDE4C
Cyclic nucleotide phosphodiesterase isoforms in human basophils and mast cells.
Peachell et al., Eşfahān, Iran. In Int J Immunopathol Pharmacol, Feb 2016
In basophils, prominent expression of mRNA for PDE4A and PDE4D was observed whereas little if any expression of PDE4B and PDE4C was detected.
Studying mechanisms of cAMP and cyclic nucleotide phosphodiesterase signaling in Leydig cell function with phosphoproteomics.
Ong et al., Washington, D.C., United States. In Cell Signal, Dec 2015
We have recently shown that PDE4B and PDE4C as well as PDE8A and PDE8B are expressed in rodent Leydig cells and that combined inhibition of PDE4 and PDE8 leads to dramatically increased steroid biosynthesis.
Effects of rolipram and roflumilast, phosphodiesterase-4 inhibitors, on hypertension-induced defects in memory function in rats.
Babu et al., Chennai, India. In Eur J Pharmacol, Feb 2015
The PDE4B and PDE4D gene expression was significantly enhanced in hypertensive rats compared with sham operated however PDE4A and PDE4C remained unaltered.
Improved age determination of blood and teeth samples using a selected set of DNA methylation markers.
Decorte et al., Leuven, Belgium. In Epigenetics, 2014
From the published literature we selected 4 age-associated genes (ASPA, PDE4C, ELOVL2, and EDARADD) and determined CpG methylation levels from 206 blood samples of both deceased and living individuals (age range: 0-91 years).
Phosphodiesterase isoenzymes in the human urethra: a molecular biology and functional study.
Ückert et al., Hannover, Germany. In Eur J Pharmacol, 2014
RT-PCR analysis revealed the expression of PDE1B, PDE1C, PDE4A, PDE4C, PDE4D, PDE5A and PDE11A.
Integrated analysis using methylation and gene expression microarrays reveals PDE4C as a prognostic biomarker in human glioma.
Jiang et al., Beijing, China. In Oncol Rep, 2014
Promoter methylation and protein expression of phosphodiesterase 4C (PDE4C) was examined in different grade gliomas and the correlation between PDE4C and wild-type (WT) p53 was evaluated in glioma cell lines.
Aging of blood can be tracked by DNA methylation changes at just three CpG sites.
Wagner et al., In Genome Biol, 2013
Methylation levels at three age-related CpGs--located in the genes ITGA2B, ASPA and PDE4C--were subsequently analyzed by bisulfite pyrosequencing of 151 blood samples.
NCS 613 exhibits anti-inflammatory effects on PBMCs from lupus patients by inhibiting p38 MAPK and NF-κB signalling pathways while reducing proinflammatory cytokine production.
Rouseau et al., Sherbrooke, Canada. In Can J Physiol Pharmacol, 2013
NCS 613 treatment decreased PDE4B and upregulated PDE4C in human PBMCs from healthy donors and SLE patients.
Whole genome SNP genotyping and exome sequencing reveal novel genetic variants and putative causative genes in congenital hyperinsulinism.
Battaglia et al., Milano, Italy. In Plos One, 2012
This strategy allowed the identification of the potential causative mutations in genes implicated in the regulation of insulin secretion such as transmembrane proteins (CACNA1A, KCNH6, KCNJ10, NOTCH2, RYR3, SCN8A, TRPV3, TRPC5), cytosolic (ACACB, CAMK2D, CDKAL1, GNAS, NOS2, PDE4C, PIK3R3) and mitochondrial enzymes (PC, SLC24A6), and in four genes (CSMD1, SLC37A3, SULF1, TLL1) suggested by TDT family-based association study.
More targets, more pathways and more clues for mutant p53.
Landi et al., Pisa, Italy. In Oncogenesis, 2012
Novel p53 candidate target genes were also identified, including ARID3B, ARNT2, CLMN, FADS1, FTH1, KPNA2, LPHN2, PARD6B, PDE4C, PIAS2, PRPF40A, PYGL and RHOBTB2, involved in the metabolism, xenobiotic responses and cell differentiation.
PGE 2 desensitizes β -agonist effect on human lung fibroblast-mediated collagen gel contraction through upregulating PDE4.
Liu et al., Beijing, China. In Mediators Inflamm, 2012
Finally, indomethacin slightly inhibited PDE4C expression, while PGE2 stimulated the expression of PDE4A and -4C in human lung fibroblasts.
Isolation and characterization of smooth muscle cells from rat corpus cavernosum tissue for the study of erectile dysfunction.
Yang et al., Ch'ŏngju, South Korea. In Korean J Urol, 2012
The levels of PDE1A, PDE1B, PDE1C, PDE2A, PDE3A, PDE4A, PDE4B, PDE4C, PDE4D, and PDE5A mRNA in the RPSMCs were about 3.2-, 4.4-, 3.4-, 29.0-, 3.5-, 2.8-, 2.9-, 6.1-, 45.0-, and 6.0-fold the corresponding expression in RASMCs.
Expression profile of proinflammatory genes in neutrophil-enriched granulocytes stimulated with native anti-PR3 autoantibodies.
Sanak et al., Kraków, Poland. In J Physiol Pharmacol, 2012
In stimulated neutrophils we observed up-regulation of 13 genes (CCL2, CXCL2, VCAM1, MMP9, PLCB4, PDE4C, PLA2G4C, RAC1, RHOA, IRAK1, CACNA1D, CACNB2, PTGDR), further 11 genes were up-regulated only in some donors (IL13, PF4, IL2RG, ITGB1, CD83, PLA2G7, ALOX12, AXNA1, AXNA5, LTA4H, MCR2) yet two others (HRH3 and PLA2G2D) were up-regulated in a few samples and undetectable in others.
Phosphodiesterase 4 and its inhibitors in inflammatory diseases.
Lin et al., Taiwan. In Chang Gung Med J, 2012
Type 4 cyclic nucleotide phosphodiesterases (PDE4) are a family of low km 3',5'-cyclic adenosine monophosphate (cAMP)-specific phosphodiesterases including at least 20 isozymes encoded by four genes (PDE4A, PDE4B, PDE4C, and PDE4D) in mammals.
Disease progression in MRL/lpr lupus-prone mice is reduced by NCS 613, a specific cyclic nucleotide phosphodiesterase type 4 (PDE4) inhibitor.
Lugnier et al., Illkirch-Graffenstaden, France. In Plos One, 2011
NCS 613 is a potent inhibitor, which is more selective for the PDE4C subtype (IC₅₀= 1.4 nM) than the other subtypes (PDE4A, IC₅₀= 44 nM; PDE4B, IC₅₀= 48 nM; and PDE4D, IC₅₀= 14 nM).
Polycystin-2 and phosphodiesterase 4C are components of a ciliary A-kinase anchoring protein complex that is disrupted in cystic kidney diseases.
Igarashi et al., Dallas, United States. In Proc Natl Acad Sci U S A, 2011
findings identify PC2 and PDE4C as unique components of an AKAP complex in primary cilia and reveal a common mechanism for dysregulation of cAMP signaling in cystic kidney diseases arising from different gene mutations
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