Disease relevance of CCRIS 3331

• Twice-weekly application of 10 mumol sn-1,2-didecanoylglycerol, a nonpromoting dosing rate, for 1 week decreased cytosolic PKC activity but increased particulate PKC activity and did not produce hyperplasia [1].
• Limited promotion with the model diacylglycerol, sn-1,2-didecanoylglycerol, similarly produced an average of 10-fold more papillomas in DMBA-treated mice than in acetone-treated/sn-1,2-didecanoylglycerol-promoted TG.AC mice [2].
• Application of TPA caused edema, but sn-1,2-didecanoylglycerol had little or no effect. sn-1,2-Didecanoylglycerol was then evaluated as a complete tumor promoter utilizing the mouse skin two-stage model [3].

High impact information on CCRIS 3331

• A single application of 10 mumol sn-1,2-didecanoylglycerol, a model sn-1,2-diacylglycerol and complete tumor promoter, induced ornithine decarboxylase to an extent similar to that of 2 nmol TPA [1].
• sn-1,2-Didecanoylglycerol, a synthetic lipid second messenger and model diacylglycerol, was evaluated as a complete skin tumor promoter in CD-1 mice [4].
• A marked effect of the acyl chain length, 3-10 carbons, of symmetric sn-1,2-diacylglycerols was observed on their ability to mimic the effect of 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA). sn-1,2-Dipropanoylglycerol did not mimic the effects of PMA, but sn-1,2-didecanoylglycerol potently mimicked PMA action [5].
• By combining the above sandwich ELISA technique with the monomolecular film technique, it was possible for the first time to measure the enzymatic activity of HGL on 1,2-didecanoyl-sn-glycerol (dicaprin) monolayers as well as to determine the corresponding interfacial excess of the enzyme [6].
• By use of directing binding studies with a nondegradable anionic substrate analogue and monomolecular surface film kinetics on 1,2-didecanoyl-sn-glycerol 3-sulfate, it is shown that the aggregation process is controlled by the ionization state of the side chains of the amino acid residues at positions 6 and 17 [7].

Biological context of CCRIS 3331

• 1-Decanoyl-2-lyso-3-sn-phosphatidic acid, when added directly to platelets, induced platelet aggregation and raised intracellular Ca2+ levels at concentrations of 0.3 microM upwards, but was without effect when formed intracellularly from 1,2-didecanoylglycerol at an estimated concentration of approx. 47 microM [8].
• Pretreatment of skin with sn-1,2-didecanoylglycerol, an activator of PKC which causes translocation but no down-regulation, did not suppress EROD induction [9].
• When tested in the form of mixed films, all the disulfide compounds investigated specifically reduced the hydrolysis of 1,2-didecanoyl-sn-glycerol films by gastric lipases, but did not affect hydrolysis by pancreatic lipase [10].

Gene context of CCRIS 3331

• The mechanism of action of bovine milk lipoprotein lipase was studied by using a monomolecular film of 1,2-didecanoylglycerol [11].
• 1,2-Didecanoylglycerol (diC10) is taken up by human platelets and sequentially converted to 1,2-didecanoylphosphatidic acid (PA10) and 1,2-didecanoylphosphatidylinositol (PI10) [12].
• The use of sn-1,2-didecanoylglycerol (DG10) as stimulating agent did not result in any detectable activation of the NADPH-oxidase [13].

References