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Our research focuses on epigenetic and chromatin mechanisms in musculoskeletal disease. Our aim is to identify possible novel therapeutic intervention points by investigating epigenetic biology mechanisms in the various cell types and tissues that are of importance in the musculoskeletal system.

Musculoskeletal diseases comprise a variety of different and often unrelated inflammatory and malignant conditions constituting a considerable and often devastating burden to affected patients.

Chemical tools such as selective and cell-active inhibitors are important in understanding biological systems. Development of chemical tools for epigenetic biology is a key goal of the Epigenetic Probe Project, a public-private partnership between the Structural Genomics Consortium (SGC) and several private organisations.

By using chemical and genetic tools we approach these goals by centering the research of our group around the following thematic areas:

  • Epigenetic regulation of immune and inflammatory cell types in musculoskeletal health and disease
  • Epigenetic Mechanisms in inflammation, ageing and mesenchymal stem cells 
  • Epigenetic mechanisms in bone oncology 
  • Structural and Chemical Biology of epigenetic and metabolic enzymes 

Our group works in collaboration with SGC and other academic and private partners

The term "Epigenetics" refers to heritable phenotypic changes of an organism which are not encoded by the storage form of genetic information, the DNA sequence itself. Epigenetic mechanisms comprise modifications of DNA bases such as methylation of cytosine residues, a plethora of different posttranslational modifications of chromatin (histones), non-coding RNA as well as nuclear architecture such as nucleosome positioning.

Several epigenetic pathways exist, with the two best studied being methylation of DNA and post-transcriptional modification of histone proteins. Each epigenetic mark or modification is modified by a set of "eraser" and "writer" enzymes - for example, the marks such as methylated or acetylated residues in histones or nuclear factors are then recognised by specific "reader" domains, often found in transcriptional complexes that mediate a change in gene expression. These epigenetic marks, however, may not be stable and could rapidly change in response to stimuli (such as environmental cues), with a postulated failure of "correct" epigenetic regulation leading to the development of disease.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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