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BRUCE protein and liver disease: Chrystelle Vilfranc

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Manage episode 306792802 series 2902469
Kandungan disediakan oleh iBiology. Semua kandungan podcast termasuk episod, grafik dan perihalan podcast dimuat naik dan disediakan terus oleh iBiology atau rakan kongsi platform podcast mereka. Jika anda percaya seseorang menggunakan karya berhak cipta anda tanpa kebenaran anda, anda boleh mengikuti proses yang digariskan di sini https://ms.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 episod

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iconKongsi
 
Manage episode 306792802 series 2902469
Kandungan disediakan oleh iBiology. Semua kandungan podcast termasuk episod, grafik dan perihalan podcast dimuat naik dan disediakan terus oleh iBiology atau rakan kongsi platform podcast mereka. Jika anda percaya seseorang menggunakan karya berhak cipta anda tanpa kebenaran anda, anda boleh mengikuti proses yang digariskan di sini https://ms.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 episod

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