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BRUCE protein and liver disease: Chrystelle Vilfranc

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Manage episode 306792802 series 2902469
Innhold levert av iBiology. Alt podcastinnhold, inkludert episoder, grafikk og podcastbeskrivelser, lastes opp og leveres direkte av iBiology eller deres podcastplattformpartner. Hvis du tror at noen bruker det opphavsrettsbeskyttede verket ditt uten din tillatelse, kan du følge prosessen skissert her https://no.player.fm/legal.
Chronic liver diseases affect millions of people worldwide. By understanding how liver disease progresses, we may be able to identify new therapies that can protect the liver. Dr. Chrystelle Vilfranc studied the role of BRUCE, a protein that is known to be important in several cellular processes in our bodies, in liver disease. She found that the absence of BRUCE in mouse livers led to accelerated liver disease and higher rates of liver cancer when combined with a liver damaging compound. Furthermore, hepatocellular carcinomas that develop in the absence of BRUCE in the liver appear to have increased β-catenin activity. Loss of BRUCE may be a marker of early liver disease in humans, and rescuing BRUCE expression or activity may help stop or reverse disease in the liver.
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100 episoder

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Manage episode 306792802 series 2902469
Innhold levert av iBiology. Alt podcastinnhold, inkludert episoder, grafikk og podcastbeskrivelser, lastes opp og leveres direkte av iBiology eller deres podcastplattformpartner. Hvis du tror at noen bruker det opphavsrettsbeskyttede verket ditt uten din tillatelse, kan du følge prosessen skissert her https://no.player.fm/legal.
Chronic liver diseases affect millions of people worldwide. By understanding how liver disease progresses, we may be able to identify new therapies that can protect the liver. Dr. Chrystelle Vilfranc studied the role of BRUCE, a protein that is known to be important in several cellular processes in our bodies, in liver disease. She found that the absence of BRUCE in mouse livers led to accelerated liver disease and higher rates of liver cancer when combined with a liver damaging compound. Furthermore, hepatocellular carcinomas that develop in the absence of BRUCE in the liver appear to have increased β-catenin activity. Loss of BRUCE may be a marker of early liver disease in humans, and rescuing BRUCE expression or activity may help stop or reverse disease in the liver.
  continue reading

100 episoder

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