Exploring the role of Cyclin B1 in Tuberin StabilizationÂ
Standing
Undergraduate
Type of Proposal
Oral Research Presentation
Challenges Theme
Open Challenge
Faculty Sponsor
Dr. Lisa Porter and Dr. Elizabeth Fidalgo Da Silva
Proposal
Tuberous Sclerosis is an autosomal dominant disorder affecting approximately 1:6,000 childbirths. This disorder results from mutations in either the Tuberous Sclerosis Complex 1 or 2 (TSC1/TSC2) genes and usually results in benign tumours in various areas of the body such as the brain, kidney, skin and lungs. Hamartin, encoded by TSC1, can reveal a ubiquitin-binding site when absent, ultimately leading to Tuberin's degradation through ubiquitin-mediated proteasomal degradation. Moreover, cyclins are a vital aspect of the cell cycle and are regulatory subunits that complex with cyclin-dependent kinases (CDKs), which are serine/threonine kinases. Cyclin B1’s function isn’t entirely understood; however, it is known that it is essential for mitotic entry. The following study examines if the exogenous expression of a cell cycle protein, Cyclin B1, can recover Tuberin levels in the absence of Hamartin.
Grand Challenges
Viable, Healthy and Safe Communities
Exploring the role of Cyclin B1 in Tuberin StabilizationÂ
Tuberous Sclerosis is an autosomal dominant disorder affecting approximately 1:6,000 childbirths. This disorder results from mutations in either the Tuberous Sclerosis Complex 1 or 2 (TSC1/TSC2) genes and usually results in benign tumours in various areas of the body such as the brain, kidney, skin and lungs. Hamartin, encoded by TSC1, can reveal a ubiquitin-binding site when absent, ultimately leading to Tuberin's degradation through ubiquitin-mediated proteasomal degradation. Moreover, cyclins are a vital aspect of the cell cycle and are regulatory subunits that complex with cyclin-dependent kinases (CDKs), which are serine/threonine kinases. Cyclin B1’s function isn’t entirely understood; however, it is known that it is essential for mitotic entry. The following study examines if the exogenous expression of a cell cycle protein, Cyclin B1, can recover Tuberin levels in the absence of Hamartin.