Faculty Profile
Name: Daiqing Liao
Homepage: http://www.acb.med.ufl.edu/about/peopleinfo.asp?FacultyID=20
Research Interests:
Our research program focuses on understanding function and regulation of tumor suppressor p53 and its homologous transcriptional activators by viral oncogenes and cellular proteins. In one project, we are studying how adenovirus E1B 55-kDa oncoprotein impacts on p53 pathway and roles of this viral oncoprotein in cell transformation induced by adenovirus, a DNA tumor virus. We have found that the E1B 55-kDa protein inhibits p53’s functions through several distinct biochemical mechanisms including inhibition of posttranslational modifications of p53, sequestration of p53 in the cytoplasm and impairs regulation of p53 by cellular proteins. Current efforts focus on understanding how E1B 55-kDa oncoprotein represses transcription and potential role of cytoplasmic sequestration of p53 by this viral oncogene in apoptosis.



In another project, we are investigating the interplay between acetylase and coactivator PCAF and p53 family of proteins and the impact of their interactions on expression of p53 target genes and on tumor suppression.



We are also interested in understanding how stresses relay signals to p53. To this end, we have found that p53 is phosphorylated at specific serine residues in the C-terminal regulatory domain by a yet to be identified kinase. We are making progress in identify this kinase through proteomic approaches. Our goal here is to identify this kinase and study its role in signaling pathways converging on p53.



Finally, we have been interested in understanding the interactions between p53 family proteins and Daxx. We and others have found that Daxx binds to p53 and p73. These interactions may play important roles in the diverse functions of Daxx ranging from transcriptional regulation to apoptosis, as well as cell cycle control.



Our long-term goal is to understand the cellular regulatory circuitries that govern cell growth and transformation through focused research on the p53 pathway by using cutting-edge technologies in cell biology, genomics and proteomics. We believe that such approaches will likely yield useful knowledge that will have major impact in cancer cell biology and may also have translational values in designing treatments for cancer patients.

Current Running Projects:
Medical - Oncogenes and tumor suppressors in cancer
Our research program focuses on understanding function and regulation of tumor suppressor p53 and its homologous transcriptional activators by viral oncogenes and cellular proteins. In one project, we are studying how adenovirus E1B 55-kDa oncoprotein impacts on p53 pathway and roles of this viral oncoprotein in cell transformation induced by adenovirus, a DNA tumor virus. We have found that the E1B 55-kDa protein inhibits p53’s functions through several distinct biochemical mechanisms including inhibition of posttranslational modifications of p53, sequestration of p53 in the cytoplasm and impairs regulation of p53 by cellular proteins. Current efforts focus on understanding how E1B 55-kDa oncoprotein represses transcription and potential role of cytoplasmic sequestration of p53 by this viral oncogene in apoptosis. In another project, we are investigating the interplay between acetylase and coactivator PCAF and p53 family of proteins and the impact of their interactions on expression of p53 target genes and on tumor suppression. We are also interested in understanding how stresses relay signals to p53. To this end, we have found that p53 is phosphorylated at specific serine residues in the C-terminal regulatory domain by a yet to be identified kinase. We are making progress in identify this kinase through proteomic approaches. Our goal here is to identify this kinase and study its role in signaling pathways converging on p53. Finally, we have been interested in understanding the interactions between p53 family proteins and Daxx. We and others have found that Daxx binds to p53 and p73. These interactions may play important roles in the diverse functions of Daxx ranging from transcriptional regulation to apoptosis, as well as cell cycle control. Our long-term goal is to understand the cellular regulatory circuitries that govern cell growth and transformation through focused research on the p53 pathway by using cutting-edge technologies in cell biology, genomics and proteomics. We believe that such approaches will likely yield useful knowledge that will have major impact in cancer cell biology and may also have translational values in designing treatments for cancer patients. See: http://plaza.ufl.edu/dliao/

Requirements: Students who have taken advanced chemistry and biology courses such as biochemistry, molecular biology, and molecular genetics.

Time Commitment:
Independent Study: Available
Work Study: Available
Salary: Not Available
Volunteer: Available
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