Papers on
PDE1C
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.
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.
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.
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.