|Source:||The herbs of Rehmannia glutinosa|
|Biological Activity or Inhibitors:||1. Biosynthesis of D-arabinose in mycobacteria - a novel bacterial pathway with implications for antimycobacterial therapy.
|Solvent:||Pyridine, Methanol, Ethanol, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||6.6622 mL||33.3111 mL||66.6223 mL||133.2445 mL||166.5556 mL|
|5 mM||1.3324 mL||6.6622 mL||13.3245 mL||26.6489 mL||33.3111 mL|
|10 mM||0.6662 mL||3.3311 mL||6.6622 mL||13.3245 mL||16.6556 mL|
|50 mM||0.1332 mL||0.6662 mL||1.3324 mL||2.6649 mL||3.3311 mL|
|100 mM||0.0666 mL||0.3331 mL||0.6662 mL||1.3324 mL||1.6656 mL|
FEBS J. 2008 Jun;275(11):2691-711.
|Biosynthesis of D-arabinose in mycobacteria - a novel bacterial pathway with implications for antimycobacterial therapy.[Pubmed: 18422659 ]|
|Decaprenyl-phospho-arabinose (beta-D-arabinofuranosyl-1-O-monophosphodecaprenol), the only known donor of D-Arabinose in bacteria, and its precursor, decaprenyl-phospho-ribose (beta-D-ribofuranosyl-1-O-monophosphodecaprenol), were first described in 1992. En route to D-arabinofuranose, the decaprenyl-phospho-ribose 2'-epimerase converts decaprenyl-phospho-ribose to decaprenyl-phospho-arabinose, which is a substrate for arabinosyltransferases in the synthesis of the cell-wall arabinogalactan and lipoarabinomannan polysaccharides of mycobacteria. The first step of the proposed decaprenyl-phospho-arabinose biosynthesis pathway in Mycobacterium tuberculosis and related actinobacteria is the formation of D-ribose 5-phosphate from sedoheptulose 7-phosphate, catalysed by the Rv1449 transketolase, and/or the isomerization of d-ribulose 5-phosphate, catalysed by the Rv2465 d-ribose 5-phosphate isomerase. d-Ribose 5-phosphate is a substrate for the Rv1017 phosphoribosyl pyrophosphate synthetase which forms 5-phosphoribosyl 1-pyrophosphate (PRPP).|
Arch Biochem Biophys. 2002 Feb 15;398(2):229-39.
|Biosynthesis of d-arabinose in Mycobacterium smegmatis: specific labeling from d-glucose.[Pubmed: 11831854 ]|
|D-Arabinose is a major sugar in the cell wall polysaccharides of Mycobacterium tuberculosis and other mycobacterial species. The reactions involved in the biosynthesis and activation of D-Arabinose represent excellent potential sites for drug intervention since D-Arabinose is not found in mammalian cells, and the cell wall arabinomannan and/or arabinogalactan appear to be essential for cell survival. Since the pathway involved in conversion of d-glucose to D-Arabinose is unknown, we incubated cells of Mycobacterium smegmatis individually with [1-(14)C]glucose, [3,4-(14)C]glucose, and [6-(14)C]glucose and compared the specific activities of the cell wall-bound arabinose. Although the specific activity of the arabinose was about 25% lower with [6-(14)C]glucose than with other labels, there did not appear to be selective loss of either carbon 1 or carbon 6, suggesting that arabinose was not formed by loss of carbon 1 of glucose via the oxidative step of the pentose phosphate pathway, or by loss of carbon 6 in the uronic acid pathway.|