Drosophila as a model for JAK/STAT associated disease
|Dates:||9 June 2015|
|Times:||15:30 - 17:00|
|What is it:||Seminar|
|Organiser:||Faculty of Life Sciences|
|Who is it for:||University staff|
The JAK/STAT signal transduction cascade is named after its components, the Janus Kinase (JAK) and the downstream transcription factor termed STAT. Normally required for a wide range of developmental, haematological and immunological processes, developments over recent years have also implicated the JAK/STAT pathway in a number of human diseases. Probably the best characterised of these are the myeloproliferative neoplasms – a class of low grade haematological malignancies characterised by an excess of erythrocytes or thrombocytes. A large proportion of these patients have been shown to have dominant gain-of-function mutations in JAK2 – a mutation which is central to the development and pathology of these diseases. Essentially incurable, newly developed JAK inhibitors offer symptomatic relief but do not appear to halt disease progression.
I will describe work being undertaken in my lab which uses novel fly-based models of JAK/STAT signalling in haematopoiesis. Our work attempts to better understand the pathway and seeks to identify genes and small molecules that might ultimately prove therapeutically relevant in human patients.
Organisation: University of Sheffield
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AV Hill Building