dc.contributor.author | Cato, L | |
dc.contributor.author | Neeb, A | |
dc.contributor.author | Sharp, A | |
dc.contributor.author | Buzón, V | |
dc.contributor.author | Ficarro, SB | |
dc.contributor.author | Yang, L | |
dc.contributor.author | Muhle-Goll, C | |
dc.contributor.author | Kuznik, NC | |
dc.contributor.author | Riisnaes, R | |
dc.contributor.author | Nava Rodrigues, D | |
dc.contributor.author | Armant, O | |
dc.contributor.author | Gourain, V | |
dc.contributor.author | Adelmant, G | |
dc.contributor.author | Ntim, EA | |
dc.contributor.author | Westerling, T | |
dc.contributor.author | Dolling, D | |
dc.contributor.author | Rescigno, P | |
dc.contributor.author | Figueiredo, I | |
dc.contributor.author | Fauser, F | |
dc.contributor.author | Wu, J | |
dc.contributor.author | Rottenberg, JT | |
dc.contributor.author | Shatkina, L | |
dc.contributor.author | Ester, C | |
dc.contributor.author | Luy, B | |
dc.contributor.author | Puchta, H | |
dc.contributor.author | Troppmair, J | |
dc.contributor.author | Jung, N | |
dc.contributor.author | Bräse, S | |
dc.contributor.author | Strähle, U | |
dc.contributor.author | Marto, JA | |
dc.contributor.author | Nienhaus, GU | |
dc.contributor.author | Al-Lazikani, B | |
dc.contributor.author | Salvatella, X | |
dc.contributor.author | de Bono, JS | |
dc.contributor.author | Cato, AC | |
dc.contributor.author | Brown, M | |
dc.date.accessioned | 2017-11-24T10:48:37Z | |
dc.date.issued | 2017-08-10 | |
dc.identifier.citation | eLife, 2017, 6 | |
dc.identifier.issn | 2050-084X | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/945 | |
dc.identifier.eissn | 2050-084X | |
dc.identifier.doi | 10.7554/elife.27159 | |
dc.description.abstract | Targeting the activation function-1 (AF-1) domain located in the N-terminus of the androgen receptor (AR) is an attractive therapeutic alternative to the current approaches to inhibit AR action in prostate cancer (PCa). Here we show that the AR AF-1 is bound by the cochaperone Bag-1L. Mutations in the AR interaction domain or loss of Bag-1L abrogate AR signaling and reduce PCa growth. Clinically, Bag-1L protein levels increase with progression to castration-resistant PCa (CRPC) and high levels of Bag-1L in primary PCa associate with a reduced clinical benefit from abiraterone when these tumors progress. Intriguingly, residues in Bag-1L important for its interaction with the AR AF-1 are within a potentially druggable pocket, implicating Bag-1L as a potential therapeutic target in PCa. | |
dc.format | Electronic | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | ELIFE SCIENCES PUBLICATIONS LTD | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | |
dc.subject | Humans | |
dc.subject | Prostatic Neoplasms | |
dc.subject | DNA-Binding Proteins | |
dc.subject | Receptors, Androgen | |
dc.subject | Transcription Factors | |
dc.subject | Protein Binding | |
dc.subject | Male | |
dc.subject | Androgen Receptor Antagonists | |
dc.subject | Protein Interaction Maps | |
dc.title | Development of Bag-1L as a therapeutic target in androgen receptor-dependent prostate cancer. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2017-08-07 | |
rioxxterms.versionofrecord | 10.7554/elife.27159 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by/4.0 | |
rioxxterms.licenseref.startdate | 2017-08-10 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | eLife | |
pubs.notes | No embargo | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Therapeutics | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Computational Biology and Chemogenomics | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies/Prostate Cancer Targeted Therapy Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies/Translational Therapeutics | |
pubs.organisational-group | /ICR/Primary Group/Royal Marsden Clinical Units | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Therapeutics | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Computational Biology and Chemogenomics | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies/Prostate Cancer Targeted Therapy Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies/Translational Therapeutics | |
pubs.organisational-group | /ICR/Primary Group/Royal Marsden Clinical Units | |
pubs.publication-status | Published | |
pubs.volume | 6 | |
pubs.embargo.terms | No embargo | |
icr.researchteam | Computational Biology and Chemogenomics | |
icr.researchteam | Prostate Cancer Targeted Therapy Group | |
icr.researchteam | Translational Therapeutics | |
dc.contributor.icrauthor | Sharp, Adam | |
dc.contributor.icrauthor | Nava Rodrigues, Daniel | |
dc.contributor.icrauthor | Rescigno, Pasquale | |
dc.contributor.icrauthor | Al-Lazikani, Bissan | |
dc.contributor.icrauthor | De Bono, Johann | |