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Small-molecule antagonists of the oncogenic Tcf/beta-catenin protein complex.

TLDR
These compounds meet predicted criteria for disrupting Tcf/beta-catenin complexes and define a general standard to establish mechanism-based activity of small molecule inhibitors of this pathogenic protein-protein interaction.
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Small-molecule antagonists of the oncogenic Tcf/β-catenin protein complex

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Small molecule blockade of transcriptional coactivation of the hypoxia-inducible factor pathway.

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Regio- and stereoselective metabolism of two C19 steroids by five highly purified and reconstituted rat hepatic cytochrome P-450 isozymes.

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Activation and inhibition of benzo(a)pyrene and aflatoxin B1 metabolism in human liver microsomes by naturally occurring flavonoids.

TLDR
The results suggest that the inhibitory effects of quercetin, morin, and kaempferol on monooxygenase activity may be caused at least in part by an inhibition in the reduction of cytochrome P-450.
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Mutagenesis of the Ha-ras oncogene in mouse skin tumors induced by polycyclic aromatic hydrocarbons.

TLDR
Mutation of the 61st codon of the Ha-ras-1 gene appears to be a critical step in the formation of mouse skin tumors induced in both of the two models tested, and two other classes of hydrocarbon-induced carcinomas are delineated--namely, tumors whose DNAs efficiently transform 3T3 cells but do not contain mutated ras genes and tumors whoseDNAs do not transform 3 T3 cells.
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NMR strategy for unraveling structures of bioactive sponge-derived oxy-polyhalogenated diphenyl ethers.

TLDR
During dereplication, a systematic method for analyzing this class of compounds was established, governed by trends in the (1)H and (13)C NMR shifts of the aromatic rings, and the success of the strategy was checked by X-ray crystal structure analysis.
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Tumorigenicity of enantiomers of chrysene 1,2-dihydrodiol and of the diastereomeric bay-region chrysene 1,2-diol-3,4-epoxides on mouse skin and in newborn mice.

TLDR
The high tumorigenic activity of (-)-chrysene 1,2-dihydrodiol and (+)-diol-epoxide 2 on mouse skin and in newborn mice indicate that these compounds are, respectively, proximate and ultimate carcinogenic metabolites of chrysene.
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Inhibition of the mutagenicity of bay-region diol epoxides of polycyclic aromatic hydrocarbons by naturally occurring plant phenols: exceptional activity of ellagic acid.

  • A. WoodM. Huang A. Conney
  • Chemistry, Biology
    Proceedings of the National Academy of Sciences…
  • 1 September 1982
TLDR
It is demonstrated that ellagic acid is a potent antagonist of the adverse biological effects of the ultimate carcinogenic metabolites of several polycyclic aromatic hydrocarbons and suggested that this naturally occurring plant phenol, normally ingested by humans, may inhibit the carcinogenicity of poly cyclic aromaticHydrocarbons.
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Inhibition of the mutagenicity of bay-region diol-epoxides of polycyclic aromatic hydrocarbons by phenolic plant flavonoids.

TLDR
Myricetin, robinetin and luteolin inhibited the mutagenic activity resulting from the metabolic activation of benzo[a]-pyrene and (+/-)-trans-7,8-dihydroxy-7-8-catechin, genistein, kaempferide and chrysin by rat liver microsomes.
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