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Role of Atg7 in Liver Damage and Regeneration

Subject Area Gastroenterology
Cell Biology
Term from 2014 to 2022
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 262580368
 
Autophagy is a principal cell survival mechanism that sustains cellular homeostasis and provides substrates for energy generation. It is involved in multiple physiological processes and numerous phatological conditions such as cancer. In the liver, autophagy regulates protein degradation and contributes as adaptation mechanism during starvation. Additionally, autophagy helps to clear toxic molecules preventing neoplastic formation. Nevertheless, until today, autophagy has a bi-functional role in cancer development: it can prevent tumor formation in normal cells and can promote survival of cancer cells. However, several mechanisms of how autophagy modulates tumor initiation and progression are still unexplained. Therefore, more basic research is needed to further understand the mechanism of autophagy modulation and to explore future applications of autophagy regulation to the treatment of liver diseases. Consequently, the aim of this project is to study the importance of Atg7 in regeneration, tumor formation and immune system in the liver. Atg7 is an essential autophagy protein indispensable mediator for autophagosome biogenesis. Using Atg7-deficient mice, we plan to deeply investigate the interaction of Chk2/p53/p21 pathway with Atg7 in proliferation of hepatocytes and hepatic progenitor cells as well as modulation of immune system during acute, moderate and chronic liver injury.
DFG Programme Research Grants
 
 

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