Coordinatore | THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
Nazionalità Coordinatore | United Kingdom [UK] |
Sito del progetto | http://www.alpha-man.eu/index.htm |
Totale costo | 1˙500˙345 € |
EC contributo | 1˙500˙345 € |
Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | ERC-2009-StG |
Funding Scheme | ERC-SG |
Anno di inizio | 2009 |
Periodo (anno-mese-giorno) | 2009-10-01 - 2014-09-30 |
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1 |
CANCER RESEARCH UK
Organization address
address: ST JOHN STREET 407 ANGEL BUILDING contact info |
UK (LONDON) | beneficiary | 768˙796.50 |
2 |
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Organization address
address: The Old Schools, Trinity Lane contact info |
UK (CAMBRIDGE) | hostInstitution | 731˙548.50 |
3 |
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Organization address
address: The Old Schools, Trinity Lane contact info |
UK (CAMBRIDGE) | hostInstitution | 731˙548.50 |
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
'Estrogen Receptor (ER) drives proliferation in breast cancers and drugs such as tamoxifen and Aromatase Inhibitors, that target ER activity, are first line treatments in clinical practice. However drug resistance is a significant clinical problem. My laboratory has reported that chromatin-modifying pioneer factors are required for ER to bind the genome, and may constitute a unique opportunity for treating drug resistant cancer. My proposal consists of two complementary approaches to comprehensively explore how Estrogen Receptor interacts with these factors to direct transcription. (1) We will demonstrate that FoxA1 and the Groucho protein TLE1 are critical mediators of ER-chromatin interactions by mapping TLE1 binding sites on a genome-wide basis, and functionally testing the roles these factors play with ER in genomic remodeling, gene transcription, cell proliferation, and endocrine resistance. (2) More globally, to characterise ER transcriptional partners on a molecular basis, we will identify the complete complement of ER-associated proteins using novel proteomic approaches. Taken together, these approaches will explore how ER employs pioneer factors mechanistically, and will identify other potential players.'