Emma Baker
Stem Cell Regulation Unit, St Vincent's Institute, Fitzroy, VIC, Australia F1000 Associate Faculty Member (since 27 May 2010)BIOGRAPHY
Emma Baker is an Associate Faculty Member who works with Faculty Member Louise Purton to recommend the scientific literature in their field.
ACADEMIC POSITION:Post-doctoral Research Fellow
EDUCATION:
• 2004 PhD, Peter MaCallum Cancer Centre, Gene Regulation Group Cancer Immunology Program & Department of Pathology, University of Melbourne
• 1999 1ST Class Honours, Bachelor of Science Honours Degree (BSc Hons), Flinders University of South Australia
• 1998 Bachelor of Science Degree (BSc), Flinders University of South Australia
AWARDS:
• 2007 NHMRC Peter Doherty Fellowship
• 2004 Lyonel and Joanna Middows Fellowship, Baker Medical Research Institute
• 2003 Oral Presentation award, Lorne Genome Conference
• 2003 International Travel Award Peter MacCallum Cancer Center
• 2002 International Travel Scholarship University of Melbourne
• 2001 Medibank Private National Young Researcher Award ($5000)
• 2000 Australian Postgraduate Award Scholarship
• 1999 Chancellors Award for outstanding academic achievement in BSc Hons
RESEARCH INTERESTS:
Osteoblasts have been identified to play significant roles in bone homeostasis and haematopoietic stem cell functions within the bone marrow. Disruption of their functional capacities is predicted to have many disease causing effects, and the correctly defined lineage commitment of osteoblasts is predicted to be a key parameter for specific roles. Specific epigenetic signatures, including histone modification and DNA methylation patterns, determine correct lineage commitment and normal cell function by governing gene expression patterns. Disruption of these patterns has been implicated in contributing to many disease states. Very little is known of the epigenetic signatures that define commitment to the osteoblast lineage, which is the major aim of my research. Specifically, I aim to examine genome wide histone modification patterns that are representative of repressive and active gene transcription, and compare this to the binding targets of some of the major transcription factors required for osteoblast commitment.
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