According to Friedrich Frischknecht, malaria parasites need to be motile at several stages during their roundabout journey, but can also be sessile for long periods. Currently, his lab is trying to understand how the parasite manages to achieve the rapid motility necessary for these first steps of infection. To this end, the scientists generate transgenic parasites that either lack certain genes or express modified forms of them. But they also use biophysical methods, in collaboration with colleagues from the physics department, to measure forces that parasites can produce. Finally, the group has generated transgenic parasites that arrest during their development in the liver to examine their potential as experimental vaccines.
Jan Siemens and his group study the molecular mechanisms underlying temperature-detection and core body temperature regulation. With their approach, which comprises methods from the fields of molecular biology, biochemistry and genetics, they were able to uncover a mechanism that might be able to decrease the heightened sensitivity of the capsaicin receptor TRPV1 without blocking it completely: not a ‘stop’, but rather a controlled ‘go’. TRPV1 is responsible for the sensitization of pain. The scientists identified another receptor – the GABAB1 receptor – that acts as partner to the capsaicin receptor and proved that the activation of this second receptor specifically prevents and counteracts sensitization of the capsaicin receptor without interfering with important regulating processes in the body. Future studies will have to reveal whether these promising findings hold any potential for analgesic treatment and/or the prevention of inflammatory pain.
Ruperto Carola is published twice a year since 2010. Members of CellNetworks have contributed in nearly every edition from the beginning. The articles are in German with a short English summary.
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