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Updated: Aug 20, 2026

Utilizing Thermal Shift Assay to Probe Substrate Binding to Selenoprotein O
Published on: August 9, 2024
Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply
Ulrich Schweizer1, Florian Streckfuss, Paco Pelt
1Neurobiologie des Selens, Neurowissenschaftliches Forschungszentrum, Charité-Universitätsmedizin Berlin, Schumannstrasse 20/21, 10117 Berlin, Germany. ulrich.schweizer@charite.de
Abstract:
Liver-specific inactivation of Trsp, the gene for selenocysteine tRNA, removes SePP (selenoprotein P) from plasma, causing serum selenium levels to fall from 298 microg/l to 50 microg/l and kidney selenium to decrease to 36% of wild-type levels. Likewise, glutathione peroxidase activities decreased in plasma and kidney to 43% and 18% respectively of wild-type levels. This agrees nicely with data from SePP knockout mice, supporting a selenium transport role for hepatically expressed SePP. However, brain selenium levels remain unaffected and neurological defects do not occur in the liver-specific Trsp knockout mice, while SePP knockout mice suffer from neurological defects. This indicates that a transport function in plasma is exerted by hepatically derived SePP, while in brain SePP fulfils a second, hitherto unexpected, essential role.
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