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Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
Oncogenic Viral Protein Interactions with p53 Family Proteins
Background:
Cellular transformation induced by oncogenic viruses is a complex process including viral molecules, host cells and environmental factors. Viruses alone are unable to reproduce and thus they need a host to use their signalling, proteosynthetic and metabolic pathways. One target host molecule is the p53 tumour suppressor. Viral proteins functionally inactivate p53 and deregulate the expression of proteins active during apoptosis, cell proliferation and DNA damage response. Hepatitis virus B HbX protein and hepatitis virus C proteins NS2 and NS5A interact with p53 and prevent its localisation to the nucleus and thus reduce its transcriptional activity. Another mechanism lies in elevated p53 degradation caused by the BZLF1 protein of the Epstein-Barr virus, the LANA protein of the Kaposi sarcoma virus and human papilloma virus E6. The Merkel cell polyomavirus large T antigen does not interact directly with p53, however it acts through downregulation of p53 mediated transcription. The tax protein of human T cell lymphotropic virus type 1 modifies p53 posttranslationally and thus blocks its interaction with other factors of transcription machinery. Due to its tumour suppressor function and role in the maintenance of the genome integrity, the p53 protein is one of the best studied proteins. Following this, evolutionary homologues with important developmental functions p63 and p73 are intensively studied as well. Their roles in oncogenesis have not been clarified yet.
Purpose:
This review describes some of their known interactions with oncogenic viral proteins.
Insights
Oncogenic viruses hijack host cells, using viral proteins to inactivate the crucial p53 tumor suppressor. This review details viral protein interactions that disrupt p53 function, impacting cell processes and potentially leading to cancer.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Cellular transformation involves viral molecules, host cells, and environmental factors.
- Viruses require host pathways for replication, targeting key molecules like p53.
- p53 is a critical tumor suppressor involved in DNA damage response and apoptosis.
Purpose of the Study:
- This review focuses on interactions between oncogenic viral proteins and the p53 tumor suppressor.
- It aims to elucidate mechanisms by which viruses disrupt p53 function.
- The review also briefly touches upon related p63 and p73 proteins.
Main Methods:
- Literature review of studies on viral protein interactions with p53.
- Analysis of molecular mechanisms of p53 inactivation by viral proteins.
- Comparative examination of different viruses and their strategies to target p53.
Main Results:
- Viral proteins inactivate p53 through various mechanisms, including direct interaction, degradation, and transcriptional downregulation.
- Examples include Hepatitis B virus (HBx), Hepatitis C virus (NS2, NS5A), Epstein-Barr virus (BZLF1), and Human Papillomavirus (E6).
- Some viral proteins, like Merkel cell polyomavirus large T antigen and HTLV-1 Tax, affect p53 indirectly.
Conclusions:
- Oncogenic viruses employ diverse strategies to neutralize p53's tumor-suppressive functions.
- Understanding these interactions is crucial for comprehending viral oncogenesis.
- Further research is needed to clarify the roles of p53 homologues (p63, p73) in cancer.
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