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1 uct (+)-menthofuran and its intermediate (+)-pulegone).
2  in 16 steps from commercially available (R)-pulegone.
3  from the commercially available terpene (S)-pulegone.
4 uran itself might influence the reduction of pulegone.
5 -methylcyclohex-2-ene-1-one (1) from (R)-(+)-pulegone (3), proceeding in 44% overall yield, is descri
6 ative in vitro anti-proliferative effects of pulegone against cervical cancer.
7 een accomplished in 10 steps each from R-(+)-pulegone, allowing assignment of the absolute configurat
8                           Menthol, menthone, pulegone and eucalyptol were identified as the major com
9 ential oil were isomenthone, neo-isomenthol, pulegone and isomenthol, constituting 34.07%, 7.65%, 19.
10 tents of the potential hepatotoxic compounds pulegone and menthofuran were reduced by <=30 % and 10 %
11 mulation of the branchpoint intermediate (+)-pulegone and the side product (+)-menthofuran.
12 coumarin, estragole, methyl-eugenol, (R)-(+)-pulegone and thujone were EU-regulated substances detect
13 f HeLa cells was dramatically increased with pulegone at a dose of 10 uM with no cytotoxic effect on
14                                        Thus, pulegone can be used as a potent therapeutic option eith
15    Similarly, the reaction of triply labeled pulegone clearly shows that the label in the product is
16 r decreased reductase activity and increased pulegone content.
17 n prepared by dynamic kinetic reduction of a pulegone-derived beta-keto ester.
18                                       From a pulegone-derived building block, a key propellane interm
19             The present study portrayed that pulegone has potential anti-proliferative activities aga
20                    The anticancer effects of pulegone in conjunction with conventional chemotherapy p
21 t of menthofuran, such that menthofuran, and pulegone increased, or decreased, in concert.
22                                          (+)-Pulegone is a central intermediate in the biosynthesis o
23 a demonstrate that the metabolic fate of (+)-pulegone is controlled through transcriptional regulatio
24 scrambled, whereas the label in the starting pulegone is retained.
25   The ability to reduce both menthofuran and pulegone levels is of commercial significance in improvi
26                   To elucidate regulation of pulegone metabolism, we modified the expression of mfs u
27 ter the acute ingestion, identified 18 ng of pulegone per mL and 1 ng of menthofuran per mL.
28 of (+)-menthofuran on the branchpoint enzyme pulegone reductase (PR) were assumed.
29 uced to (-)-menthone en route to menthol, by pulegone reductase (PR), or oxidized to (+)-menthofuran,
30 tain biosynthetic enzyme concentrations [(+)-pulegone reductase and (+)-menthofuran synthase], wherea
31 ed to secretory cell mitochondria, while (+)-pulegone reductase labeling occurred only in secretory c
32 iperitenol dehydrogenase, and peppermint (+)-pulegone reductase.
33 s in all transformed plants, the flux of (+)-pulegone through PR correlated negatively with the essen
34 n of BAX was increased and BCL2 decreased in pulegone treated cells.
35 stry of P53 showed an increased apoptosis in Pulegone-treated cells compared to control and Cisplatin
36                                              Pulegone-treated HeLa cells showed an increasing degree
37                                        After pulegone treatment, fluorescent Hoechst 33,342 staining