NF-κB: a master regulator of the cellular response to stress and infection

NF-κB: a master regulator of the cellular response to stress and infection

NF-kB subunits are effectors for an incredibly diverse range of cell stimuli and stresses. Although best known for their roles in the inflammatory and immune responses NF-kB subunits also respond environmental challenges such as DNA damage, oxidative stress and hypoxia. The consequences of NF-kB activation do not fall into a 'one size fits all' category. Different genes become activated or repressed depending on a variety of contextual modulators, including the activity of parallel signalling pathways and transcription factors. My lab has been interested in the pathways that control the differential responses of NF-kB to inflammatory and DNA damage stimuli. In particular we have previously characterised how crosstalk with the p53 tumour suppressor can affect NF-kB function in cancer and how NF-kB can mediate pro-apoptotic responses following DNA replication stress (in contrast to its anti-apoptotic functions following stimulation with inflammatory cytokines). Recently we have been investigating how the NF-kB response to DNA replication stress affects its roles in mouse models of B-cell lymphoma, liver regeneration and hepatocellular carcinoma.
 
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