The Concise Guide toPHARMACOLOGY2013/14: Transporters

Abstract

The Concise Guide to PHARMACOLOGY 2013/14 provides concise overviews of the key properties of over 2000 human drug targets with their pharmacology, plus links to an open access knowledgebase of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. The full contents can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.12444/full.Transporters are one of the seven major pharmacological targets into which the Guide is divided, with the others being G protein-coupled receptors, ligand-gated ion channels, ion channels, catalytic receptors, nuclear hormone receptors and enzymes. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. A new landscape format has easy to use tables comparing related targets.It is a condensed version of material contemporary to late 2013, which is presented in greater detail and constantly updated on the website www.guidetopharmacology.org, superseding data presented in previous Guides to Receptors and Channels. It is produced in conjunction with NC-IUPHAR and provides the official IUPHAR classification and nomenclature for human drug targets, where appropriate. It consolidates information previously curated and displayed separately in IUPHAR-DB and the Guide to Receptors and Channels, providing a permanent, citable, point-in-time record that will survive database updates.

Preclinical Evaluation of 11C-Sarcosine as a Substrate of Proton-Coupled Amino Acid Transporters and First Human Application in Prostate Cancer

“…The 11 C-sarcosine uptake was determined to be 12.5% 6 1.1% of the administered dose (n 5 12). 11 C-sarcosine uptake was then determined using specific competitive inhibitors of 2 amino acid transporter systems, 5-hydroxy-L-tryptophan (HT) for the protoncoupled amino acid transporters (PAT1 gene symbol SLC36A1, PAT2 gene symbol SLC36A2, PAT4 gene symbol SLC36A4) (15) and 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) for system L (16). Thereafter, 11 C-sarcosine was added to cells for 20 min and washed 3 times before counting.…”

“…Briefly, the organ distribution of 11 C-sarcosine was determined in 2 male and 2 female Sprague-Dawley rats at 5 time points (5,15,30,60, and 90 min) using injected doses of 7.4-28 MBq of 11 C-sarcosine. Groups of animals were sacrificed while under isoflurane anesthesia.…”

“…We further determined the volatile 11 C-CO 2 fraction of radioactivity within blood, pancreas, and prostate in 1 animal per time point (15,30, and 60 min after administration). The 11 C-CO 2 fraction ranged from 14% to 21% in blood, 9% to 23% in prostate, and 12% to 24% in pancreas.…”

Domestication and early experiences in chickens: Behavior, stress and gene expression

“…RGS1 encodes a protein involved in G protein signaling (Kim et al, 2010). A number of important receptors in the pituitary gland are G protein coupled receptors (Alexander et al, 2013), and further investigations should look into whether the RGS1 protein interacts with the functioning of these, and if this is affected by stress exposure.…”

Integrin β3 mediates cerebrovascular remodelling through Src/ClC‐3 volume‐regulated Cl− channel signalling pathway

“…Interestingly, both mechanical stress and hypertrophic stimuli (Ang II, endothelin-1) activated volume-regulated Cl − currents in cardiomyocytes and vascular smooth muscle cells (VSMCs; Sato and Koumi, 1998;Shi et al, 2007;Ren et al, 2008). Our previous studies demonstrated that ClC-3 (see Alexander et al, 2013) is responsible for volume-regulated Cl − currents in VSMCs (Zhou et al, 2005) and the activity of the volumeregulated ClC-3 Cl − channel displayed a pressure-dependent increase in basilar artery smooth muscle cells (BASMCs) from 2-kidney 2-clip (2K2C) hypertensive rats, and the size of this increase paralleled the severity of cerebrovascular remodelling (Shi et al, 2007). Also, a deficiency of ClC-3 channels attenuated cerebrovascular remodelling during hypertension (Liu et al, 2010;Zheng et al, 2013).…”