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[We will resume: (i) how UGT2B15 and UGT2B17 contribute to androgen elimination; (ii) how their glucuronidation capacity influences the androgen signaling pathway in prostate cells; (iii) how they contribute to the anti-proliferative properties of AR antagonists in prostate cancer cells; and (iv) how AR and its spliced variants regulate the UGT2B15 and/or UGT2B17 genes expression.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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Gene-disease associations inferred from text-mining the literature.
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