Following my undergraduate degree in Biochemistry at Imperial College London, I joined the Kennedy Institute in 2015 for my PhD. My research interests lie in the signal transduction pathways regulating innate immune responses with a focus on the transcription factor interferon regulatory factor 5 (IRF5). IRF5 defines the pro-inflammatory phenotype of macrophages and contributes to the pathogenesis of inflammatory and autoimmune diseases including systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD) and rheumatoid arthritis (RA). Given the importance of IRF5 function in physiology and disease, IRF5 represents a new therapeutic target. One way of blocking IRF5 function is interfering with the molecular events that lead to its activation. However, the mechanism regulating IRF5 activation and the kinase responsible for its phosphorylation in vivo has been unclear. We have made inroads into this issue using a number of the state-of-the-art approaches and discovered a few novel putative IRF5 kinases. During the course of my PhD, my aims are to validate the candidate kinases, explore the substrate specificity of the identified IRF5 kinases, and investigate the effect of inhibitors of the validated kinases in controlling IRF5 activity in macrophages.
Cell shape and the microenvironment regulate nuclear translocation of NF-κB in breast epithelial and tumor cells.
Sero JE. et al, (2015), Mol syst biol, 11
Almuttaqi H. and Udalova IA., The febs journal