| Literature DB >> 29225078 |
Eva De Mol1, Elzbieta Szulc1, Claudio Di Sanza1, Paula Martínez-Cristóbal1, Carlos W Bertoncini1, R Bryn Fenwick1, Marta Frigolé-Vivas1, Marianela Masín1, Irene Hunter2, Víctor Buzón1, Isabelle Brun-Heath1, Jesús García1, Gianni De Fabritiis3, Eva Estébanez-Perpiñá4, Iain J McEwan2, Ángel R Nebreda5, Xavier Salvatella6.
Abstract
The androgen receptor is a transcription factor that plays a key role in the development of prostate cancer, and its interactions with general transcription regulators are therefore of potential therapeutic interest. The mechanistic basis of these interactions is poorly understood due to the intrinsically disordered nature of the transactivation domain of the androgen receptor and the generally transient nature of the protein-protein interactions that trigger transcription. Here, we identify a motif of the transactivation domain that contributes to transcriptional activity by recruiting the C-terminal domain of subunit 1 of the general transcription regulator TFIIF. These findings provide molecular insights into the regulation of androgen receptor function and suggest strategies for treating castration-resistant prostate cancer.Entities:
Keywords: androgen receptor; castration-resistant prostate cancer; intrinsic disorder; protein phosphorylation; protein-protein interactions; transcription; transcription factor IIF
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Year: 2017 PMID： 29225078 PMCID： PMC5830076 DOI： 10.1016/j.str.2017.11.007
Source DB: PubMed Journal: Structure ISSN： 0969-2126 Impact factor: 5.006