66394 Results for: "Ethyl-3-formyl-1H-indole-2-carboxylate&amp"

Supplier: MP Biomedicals

Citric acid is a key metabolic intermediate. Citrate is the starting point of the tricarboxylic acid cycle. Its concentration also coordinates several other metabolic pathways. Citric acid can form complexes with various cations, particularly with iron and calcium. In animals, citric acid improves the utilization of nutritional calcium. Citric acid is produced commercially by fermentation of carbohydrates derived from corn starch and from beet molasses.
Citric Acid, Trisodium Salt, Dihydrate is used as a substrate for citrate lyase, a buffer component; an anticoagulant. For anticoagulation use it is typically used at a concentration of approximately 0.129 M (i.e. for 4.5 mL blood use 16.0 mg sodium citrate and 2.1 mg citric acid).
To make a sodium citrate buffer use equimolar concentrations (typically approximately 0.05 M concentration) of citric acid, free acid and sodium citrate. Add equal volumes of each solution and titrate to the desired pH.
Room Temperature

Supplier: MP Biomedicals

β-NADP is a coenzyme necessary for the alcoholic fermentation of glucose and the oxidative dehydrogenation of other substances. It occurs widely in living tissue, especially in the liver. Nicotinic acid can be converted to nicotinamide in the body and, in this form, is found as a component of two oxidation-reduction coenzymes: nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). The nicotinamide portion of the coenzyme transfers hydrogens by alternating between oxidized quaternary nitrogen and a reduced tertiary nitrogen. NADP is an essential coenzyme for glucose-6-phosphate dehydrogenase which catalyzes the oxidation of glucose-6-phosphate to 6-phosphogluconic acid. This reaction initiates metabolism of glucose by a pathway other than the citric acid cycle. This route is known as the hexose phosphate shunt or phosphogluconate pathway. Other enzymes which utilize NADP as a coenzyme are: Alcohol dehydrogenase:NADP dependent; Aromatic ADH:NADP dependent; Ferredoxin-NADP reductase; L-Fucose dehydrogenase; Gabase; Galactose-1-phosphate uridyl transferase; Glucose dehydrogenase; L-Glutamic dehydrogenase; Glycerol dehydrogenase:NADP specific; Isocitric dehydrogenase; Malic enzymes; 5,10-Methylenetetrahydrofolate dehydrogenase; 6-Phosphogluconate dehydrogenase and Succinic semialdehyde dehydrogenase.

Supplier: MP Biomedicals

Potassium sodium tartrate tetrahydrate has been used in organic synthesis to break up emulsions in aqueous workups.

Supplier: MP Biomedicals

Arachidonic Acid is an essential fatty acid. Occurs in liver, brain, glandular organs, and depot fats of animals, in small amounts in human depot fats, and is a constituent of animal phosphatides.
Arachidonic Acid is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. Arachidonic acid plays a key role in cellular regulation and is controlled through multiple interconnected pathways.
Arachidonic acid (AA) is an unsaturated ω6 fatty acid constituent of the phospholipids of cell membranes. Phospholipase A2 releases AA from the membrane phospholipids in response to inflammation. AA is subsequently metabolized to prostaglandins and thromboxanes by at least two cyclooxygenase (COX) isoforms, to leukotrienes and lipoxins by lipoxygenases, and to epoxyeicosatrienoic acids via cytochrome p450-catalyzed metabolism. AA and its metabolites play important roles in a variety of biological processes, including signal transduction, smooth muscle contraction, chemotaxis, cell proliferation and differentiation, and apoptosis. AA has been demonstrated to bind to the a subunit of G protein and inhibit the activity of Ras GTPase-activating proteins (GAPs). Cellular uptake of AA is energy dependent and involves protein-facilitated transport across the plasma membrane.
If ethanol is undesirable, arachidonic acid may be dissolved in acetonitrile, DMF, or DMSO. Simply evaporate the ethanol under a gentle stream of nitrogen (be certain not to evaporate the material to dryness) and redissolve the arachidonic acid in the solvent of choice.Just prior to use, make dilutions of the stock solution into aqueous buffer or isotonic saline to bring the arachidonic acid to the desired concentration. Ensure that the residual amount of organic solvent is insignificant, since organic solvents may have physiologic effects at low concentrations. A control using the solvent in the absence of the prostaglandin will address this potential variable. We do not recommend storing the aqueous solution for more than one day. It is difficult to obtain aqueous solutions of arachidonic acid directly. However, an organic solvent free solution of arachidonic acid can be prepared using concentrated basic buffers (pH > 8.0 and ionic strength not less than 0.1 M). Add 400 μL of cold buffer (0 °C) per mg of arachidonic acid and agitate vigorously and/or ultrasonicate.