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Fig 1.

Structure of the tamoxifen-derived triphenylethylene scaffold with key regions of the molecule annotated.

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Fig 2.

Activity of commercially available SERM against C. neoformans and C. albicans.

The structure, molecule number used in the text, name, minimum inhibitory concentration (MIC, μg/mL) against C.neoformans (first number) and MIC against C. albicans are provided.

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Fig 3.

Antifungal activity of aryl-ring substituted tamoxifen derivatives.

The structure, molecule number used in the text, minimum inhibitory concentration (MIC, μg/mL) against C.neoformans (first number) and MIC against C. albicans are provided.

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Fig 3 Expand

Fig 4.

Antifungal activity of 2-ethenyl-substituted tamoxifen derivatives.

The structure, molecule number used in the text, minimum inhibitory concentration (MIC, μg/mL) against C.neoformans (first number) and MIC against C. albicans are provided.

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Fig 4 Expand

Fig 5.

Effect of tamoxifen-derivatives on the temperature-induced, calmodulin-dependent nuclear localization of the transcription factor Crz1.

As described in the materials and methods, C. neoformans cells harboring Crz1-mCherry and the nuclear marker Nop1-GFP were shifted to 37°C in the presence or absence of the indicated tamoxifen derivative (see Figs 24 for structures corresponding to the molecule numbers) at ¼ of minimum inhibitory concentration (MIC). The percentage of cells with co-localized mCherry and GFP signals was determined for a minimum of 100 cells with at least two independent biological samples. The bars indicate mean percentage of cells with nuclear Crz1 and error bars indicate standard deviation. All compounds except those with an asterisk (*) above the bar gave values that were significantly different than the untreated control (P< 0.05, Student’s unpaired, two-tailed t test). MIC values are taken from data in Figs 24.

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Fig 6.

Model of tamoxifen binding to Cryptococcus neoformans calmodulin.

As described in the materials and methods, a homology model of C. neoformans calmodulin bound to tamoxifen was built based on the structure of the bovine calmodulin-trifluoperazine complex [25]. A. Binding of tamoxifen to the trifluoperazine binding pocket. The numbers are arbitrary indicators of the four regions of the binding pockets described in the text. B. Overlay of tamoxifen with one molecule of trifluoperazine in the binding pocket. C. Overlay of tamoxifen with binding pocket containing both molecules of trifluoperazine.

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Fig 7.

Summary of structure-activity relationships.

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Fig 7 Expand