Babraham/European studentship: Regulation of PI3 kinase gamma in vivo

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White blood cells are an essential part of our immune systems defense against infection by bacterial and fungal pathogens. They are capable of detecting, migrating towards and destroying potential disease causing pathogens. If they become over-activated in auto-immune or sustained inflammatory disease, however, they can become causative agents in the disease process. On this basis a number of pharmaceutical companies are trying make drugs that can target the potentially bad aspects of neutrophil (a type of white blood cell) behaviour without impacting the good.
We are studying key proteins inside neutrophils that we have shown control both their ability to migrate into areas of inflammation and their ability to destroy pathogens. The protein p110 gamma is known to be a master regulator of neutrophil function controlling both their migration to sites of inflammation and their ability to kill pathogens. Importantly we have found two related protein molecules called p84 and p101 that are highly enriched in neutrophils that have many similar properties through their ability to bind to p110 gamma.
We have evidence that unexpectedly p84 and p101 can control different aspects of p110 gamma function. We have already made a genetically modified mouse line that is completely normal except it lacks p101 in its neutrophils. Now we aim to make mice lacking p84 and both p84 and p101 to complete this study. The work of of interest to the pharmaceutical sector because of the above.

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