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Adrian P. Bracken

Researcher at Trinity College, Dublin

Publications -  61
Citations -  10617

Adrian P. Bracken is an academic researcher from Trinity College, Dublin. The author has contributed to research in topics: PRC2 & Chromatin. The author has an hindex of 31, co-authored 56 publications receiving 9652 citations. Previous affiliations of Adrian P. Bracken include European Institute of Oncology & Boston Children's Hospital.

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Genome-wide mapping of Polycomb target genes unravels their roles in cell fate transitions

TL;DR: The Polycomb group (PcG) proteins form chromatin-modifying complexes that are essential for embryonic development and stem cell renewal and are commonly deregulated in cancer are identified using genome-wide location analysis in human embryonic fibroblasts.
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EZH2 is downstream of the pRB‐E2F pathway, essential for proliferation and amplified in cancer

TL;DR: It is demonstrated that both EZH2 and EED are essential for the proliferation of both transformed and non‐transformed human cells and, in addition, the pRB‐E2F pathway tightly regulates their expression and, consistent with this, it is found that EZh2 is highly expressed in a large set of human tumors.
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Suz12 is essential for mouse development and for EZH2 histone methyltransferase activity

TL;DR: It is shown that mice lacking Suz12 are not viable and die during early postimplantation stages displaying severe developmental and proliferative defects, and an essential role of SUZ12 in regulating the activity of the PRC2/3 complexes, which are required for regulating proliferation and embryogenesis.
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The Polycomb group proteins bind throughout the INK4A-ARF locus and are disassociated in senescent cells

TL;DR: The ability of the oncogene BMI1 to repress the INK4A-ARF locus requires its direct association and is dependent on the continued presence of the EZH2-containing Polycomb-Repressive Complex 2 (PRC2) complex.
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E2Fs regulate the expression of genes involved in differentiation, development, proliferation, and apoptosis

TL;DR: It is shown that the E2Fs control the expression of several genes that are involved in cell proliferation and apoptosis, differentiation, and development and provide possible genetic explanations to the variety of phenotypes observed as a consequence of a deregulated pRB/E2F pathway.