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Phosphodiesterase 1C, calmodulin-dependent 70kDa

PDE1C, phosphodiesterase 1C
Cyclic nucleotide phosphodiesterases (PDEs) catalyze hydrolysis of the cyclic nucleotides cAMP and cGMP to the corresponding nucleoside 5-prime-monophosphates. Mammalian PDEs have been classified into several families based on their biochemical properties. Members of the PDE1 family, such as PDE1C, are calmodulin (see MIM 114180)-dependent PDEs (CaM-PDEs) that are stimulated by a calcium-calmodulin complex (Repaske et al., 1992 [PubMed 1326532]).[supplied by OMIM, Oct 2009] (from NCBI)
Top mentioned proteins: Phosphodiesterase, PDE, 63-kDa, PDE4D, PDE5
Papers on PDE1C
Phosphodiesterase 1 regulation is a key mechanism in vascular aging.
Roks et al., Rotterdam, Netherlands. In Clin Sci (lond), Dec 2015
PDE1C levels were increased in lung and aorta.
Cyclic nucleotide phosphodiesterase 1 and vascular aging.
Yan, Rochester, United States. In Clin Sci (lond), Dec 2015
In the study published in the latest issue of Clinical Science, Bautista Niño and colleagues have shown that, in cultured senescent human VSMCs, PDE1A and PDE1C mRNA levels are significantly up-regulated and inhibition of PDE1 activity with vinpocetine reduced cellular senescent makers in senescent VSMCs.
An imputation-based genome-wide association study on traits related to male reproduction in a White Duroc × Erhualian F2 population.
Xing et al., Nanchang, China. In Anim Sci J, Nov 2015
We highlighted several interesting candidate genes at these loci, including APN, TEP1, PARP2, SPINK1 and PDE1C.
Modulation of Polycystic Kidney Disease Severity by Phosphodiesterase 1 and 3 Subfamilies.
Torres et al., Rochester, United States. In J Am Soc Nephrol, Oct 2015
In Pkd2(-/WS25) mice, knockout of Pde1a, Pde1c, or Pde3a but not of Pde1b or Pde3b aggravated the development of PKD and was associated with higher levels of protein kinase A-phosphorylated (Ser133) cAMP-responsive binding protein (P-CREB), activating transcription factor-1, and CREB-induced CRE modulator proteins in kidney nuclear preparations.
Role of cAMP-phosphodiesterase 1C signaling in regulating growth factor receptor stability, vascular smooth muscle cell growth, migration, and neointimal hyperplasia.
Yan et al., Houston, United States. In Circ Res, Apr 2015
We observed that PDE1C expression was low in contractile SMCs but drastically elevated in synthetic SMCs in vitro and in various mouse vascular injury models in vivo.
Cyclic nucleotide phosphodiesterase-1C (PDE1C) drives cell proliferation, migration and invasion in glioblastoma multiforme cells in vitro.
Warr et al., Wolverhampton, United Kingdom. In Mol Carcinog, Feb 2015
We previously detected focal genomic amplification of PDE1C in >90 glioblastoma multiforme (GBM) cells suggesting a potential as a novel therapeutic target in these cells.
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.
Turning on cGMP-dependent pathways to treat cardiac dysfunctions: boom, bust, and beyond.
Hofmann et al., Tübingen, Germany. In Trends Pharmacol Sci, 2014
Preclinical cardioprotection observed for sildenafil may result from inhibition of PDE5 in non-cardiomyocytes or off-target effects, possibly on PDE1C.
Postnatal odorant exposure induces peripheral olfactory plasticity at the cellular level.
Grosmaitre et al., Gif-sur-Yvette, France. In J Neurosci, 2014
Meanwhile, quantitative PCR indicates that each MOR23 neuron has higher levels of olfactory receptor transcripts and also expresses more CNGA2 and phosphodiesterase 1C, fundamental olfactory transduction pathway proteins.
Select 3',5'-cyclic nucleotide phosphodiesterases exhibit altered expression in the aged rodent brain.
Kleiman et al., Columbia, United States. In Cell Signal, 2014
PDE1B, PDE1C, PDE2A, PDE4A, PDE4D, PDE5A, PDE7A, PDE8A, PDE8B, PDE10A, and PDE11A showed an age-related increase or decrease in mRNA expression in at least 1 of the 4 brain regions examined (hippocampus, cortex, striatum, and cerebellum).
Rank-based genome-wide analysis reveals the association of ryanodine receptor-2 gene variants with childhood asthma among human populations.
Mersha et al., Cincinnati, United States. In Hum Genomics, 2012
Although the top 1,000 SNPs were not shared, 11 genes (RYR2, PDE4D, CSMD1, CDH13, ROBO2, RBFOX1, PTPRD, NPAS3, PDE1C, SEMA5A, and CTNNA2) mapped by these SNPs were shared across populations.
Cyclic nucleotide phosphodiesterase 1 regulates lysosome-dependent type I collagen protein degradation in vascular smooth muscle cells.
Yan et al., Rochester, United States. In Arterioscler Thromb Vasc Biol, 2011
Suggest that PDE1C plays a critical role in regulating collagen homeostasis during pathological vascular remodeling.
[Phosphodiesterase regulation of cardiovascular functions].
Gao et al., Beijing, China. In Sheng Li Ke Xue Jin Zhan, 2010
The expression of PDE4 and PDE1C is upregulated during proliferation of vascular smooth muscle cells.
Calcium-dependent phosphodiesterase 1C inhibits renin release from isolated juxtaglomerular cells.
Beierwaltes et al., Detroit, United States. In Am J Physiol Regul Integr Comp Physiol, 2009
PDE1C is expressed in isolated juxtaglomerular cells, and contributes to calcium's inhibitory modulation of renin release from juxtaglomerular cells.
Cyclic nucleotide phosphodiesterase PDE1C1 in human cardiac myocytes.
Movsesian et al., Salt Lake City, United States. In J Biol Chem, 2007
PDE1C1 is expressed at high levels in human cardiac myocytes with an intracellular distribution distinct from that of PDE3A
Neural upregulation in interstitial cystitis.
Gebhart et al., Vancouver, Canada. In Urology, 2007
Animal experiments have shown upregulation of proteinase-activated receptors, tryptase, beta-nerve growth factor, inducible nitric oxide synthase, nuclear transcription factor-kappaB, c-Fos, phosphodiesterase 1C, cyclic adenosine monophosphate (cAMP)-dependent protein kinase, and proenkephalin B. After the noxious stimulus has abated, downregulation of genes appears to follow.
Subcellular localization and regulation of type-1C and type-5 phosphodiesterases.
Jannini et al., Roma, Italy. In Biochem Biophys Res Commun, 2006
PDE1C levels decreased in all conditions that inhibited proliferation
Cyclic nucleotide phosphodiesterases in pancreatic islets.
Furman et al., Glasgow, United Kingdom. In Diabetologia, 2003
Several studies have shown pancreatic islets or beta cells to contain PDE1C, PDE3B and PDE4, with some evidence for PDE10A.
Cyclic GMP phosphodiesterases and regulation of smooth muscle function.
Beavo et al., Seattle, United States. In Circ Res, 2003
In humans, this decrease is caused in large part by induction of another Ca2+/calmodulin-dependent PDE (PDE1C) that allows the brake to be released and proliferation to start.
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