Dr. Tara Beattie is an Associate Professor in the Departments of Biochemistry and Molecular Biology and Oncology. She obtained her PhD from the University of Toronto in 1997 and completed her post-doctoral training with Dr. Lea Harrington and the Ontario Cancer Institute from 1997-2000. In 2001, she became anindependent investigator at the University of Calgary in the Cumming School of Medicine.
Beattie, Tara
Fundamental Research
Professor
Biography
Area of Focus
- Functional Interactions within the human telomerase complex.
- Role of DNA repair proteins in telomere
Summary of Research
Dr. Beattie’s lab focuses on telomere integrity and the enzyme telomerase as a critical factor in the progression of age-related diseases. Telomeres are specialized structures that form the protective ends of linear chromosomes. Telomeres confer stability of our DNA and therefore, telomere structure needs to be maintained in cells, since changes in DNA integrity can lead to multiple disease states. Activation of the enzyme telomerase, which maintains telomere length in dividing cells, is essential for the unregulated growth of many cancer cells. However, in addition there are at least four three disease states that arise from mutations in telomerase, stressing the importance of the delicate balance that must be preserved between telomerase activation and telomerase inhibition – either too much, or too little of the enzyme can be bad for the cell.
Area Of Focus
- Functional Interactions within the human telomerase complex.
- Role of DNA repair proteins in telomere
Summary Of Research
Dr. Beattie’s lab focuses on telomere integrity and the enzyme telomerase as a critical factor in the progression of age-related diseases. Telomeres are specialized structures that form the protective ends of linear chromosomes. Telomeres confer stability of our DNA and therefore, telomere structure needs to be maintained in cells, since changes in DNA integrity can lead to multiple disease states. Activation of the enzyme telomerase, which maintains telomere length in dividing cells, is essential for the unregulated growth of many cancer cells. However, in addition there are at least four three disease states that arise from mutations in telomerase, stressing the importance of the delicate balance that must be preserved between telomerase activation and telomerase inhibition – either too much, or too little of the enzyme can be bad for the cell.