Ulrich Schweizer

SELECTIVE RESTORATION OF THE SELENOPROTEIN POPULATION IN A MOUSE HEPATOCYTE SELENOPROTEINLESS BACKGROUND WITH DIFFERENT MUTANT SELENOCYSTEINE tRNAs LACKING (2007)

Carlson, Bradley A., Moustafa, Mohamed E., Sengupta, Aniruddha, Schweizer, Ulrich, Shrimali, Rajeev, Rao, Mahadev, ...

Novel mouse models were developed in which the hepatic selenoprotein population was targeted for removal by disrupting the selenocysteine (Sec) tRNA [Ser]Sec gene (trsp) and then selenoprotein...

Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply

Schweizer, Ulrich, Streckfuß, Florian, Pelt, Paco, Carlson, Bradley A., Hatfield, Dolph L., Köhrle, Josef, ...

Liver-specific inactivation of Trsp, the gene for selenocysteine tRNA, removes SePP (selenoprotein P) from plasma, causing serum selenium levels to fall from 298 μg/l to 50 μg/l and kidney...

Gene disruption discloses role of selenoprotein P in selenium delivery to target tissues.

Schomburg, Lutz, Schweizer, Ulrich, Holtmann, Bettina, Flohé, Leopold, Sendtner, Michael, Köhrle, Josef

Selenoprotein P (SePP), the major selenoprotein in plasma, has been implicated in selenium transport, selenium detoxification or antioxidant defence. We generated SePP-knockout mice that were viable,...

Efficient selenium transfer from mother to offspring in selenoprotein-P-deficient mice enables dose-dependent rescue of phenotypes associated with selenium deficiency.

Schweizer, Ulrich, Michaelis, Marten, Köhrle, Josef, Schomburg, Lutz

Mice deficient in selenoprotein P exhibit a disturbed selenium distribution and reduced activities of other selenoenzymes and display defects in growth and motor co-ordination. We have normalized...

Essential role of Bag-1 in differentiation and survival of hematopoietic and neuronal cells

Götz, Rudolf, Wiese, Stefan, Takayama, Shinichi, Camarero, Guadalupe C., Rossoll, Wilfried, Schweizer, Ulrich, ...

By targeted gene disruption in mice, we show that Bag-1, a co-chaperone for Hsp70 which interacts with C-Raf, B-Raf, Akt, Bcl-2, steroid hormone receptors and other proteins, plays an essential role...

Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply

Schweizer, Ulrich, Streckfuß, Florian, Pelt, Paco, Carlson, Bradley A., Hatfield, Dolph L., Köhrle, Josef, ...

Liver-specific inactivation of Trsp, the gene for selenocysteine tRNA, removes SePP (selenoprotein P) from plasma, causing serum selenium levels to fall from 298 μg/l to 50 μg/l and kidney...

Gene disruption discloses role of selenoprotein P in selenium delivery to target tissues.

Schomburg, Lutz, Schweizer, Ulrich, Holtmann, Bettina, Flohé, Leopold, Sendtner, Michael, Köhrle, Josef

Selenoprotein P (SePP), the major selenoprotein in plasma, has been implicated in selenium transport, selenium detoxification or antioxidant defence. We generated SePP-knockout mice that were viable,...

Efficient selenium transfer from mother to offspring in selenoprotein-P-deficient mice enables dose-dependent rescue of phenotypes associated with selenium deficiency.

Schweizer, Ulrich, Michaelis, Marten, Köhrle, Josef, Schomburg, Lutz

Mice deficient in selenoprotein P exhibit a disturbed selenium distribution and reduced activities of other selenoenzymes and display defects in growth and motor co-ordination. We have normalized...

The Role of Thioredoxin Reductases in Brain Development

Soerensen, Jonna, Jakupoglu, Cemile, Beck, Heike, Förster, Heidi, Schmidt, Jörg, Schmahl, Wolfgang, ...

The thioredoxin-dependent system is an essential regulator of cellular redox balance. Since oxidative stress has been linked with neurodegenerative disease, we studied the roles of thioredoxin...

Conditional gene ablation of Stat3 reveals differential signaling requirements for survival of motoneurons during development and after nerve injury in the adult

Schweizer, Ulrich, Gunnersen, Jennifer, Karch, Christoph, Wiese, Stefan, Holtmann, Bettina, Takeda, Kiyoshi, ...

Members of the ciliary neurotrophic factor (CNTF)/leukemia inhibitory factor (LIF)/cardiotrophin gene family are potent survival factors for embryonic and lesioned motoneurons. These factors act via...