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The variability of the C-terminal domain of GSTs enables these enzymes to use a variety of substrates to bind activated glutathione to most hydrophobic compounds containing electrophilic atoms [4]

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We then attempted to soak the NMR hit ( 27 ) and its analogues ( 2834 ) into the TRF1 TRFH crystals to validate the binding mode of the series

Understanding the metabolic mechanisms underlying breast cancer metastasis will provide important clues to develop novel therapeutic approaches for treatment of metastatic breast cancer

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