| Type of Document |
Master's Thesis |
| Author |
Valentin-Santiago, Mayda
|
| Author's Email Address |
mayda.valentin@vanderbilt.edu |
| URN |
etd-03302007-143206 |
| Title |
Role of Autophagy in BCL-2/BCL-XL Mediated G0 Arrest |
| Degree |
Master of Science |
| Department |
Cancer Biology |
| Advisory Committee |
| Advisor Name |
Title |
| Elizabeth Yang |
Committee Chair |
| Pran Datta |
Committee Member |
|
| Keywords |
- Bcl-xL
- cell cycle
- autophagy
- Bcl-2
- Apoptosis -- Molecular aspects
|
| Date of Defense |
2007-03-29 |
| Availability |
unrestricted |
Abstract
Although many studies have investigated the pro- and anti-apoptotic functions of the Bcl-2 family of proteins, it has been found that the anti-apoptotic Bcl-2 and Bcl-xL molecules also have a role in the cell cycle. It has been shown that cells that overexpress either Bcl-2 or Bcl-xL exhibit enhanced cell cycle arrest upon serum starvation or contact inhibition. The characteristic cell cycle arrest phenotype observed in Bcl-2 or Bcl-xL expressing cells resembles the autophagy-induced cell cycle arrest. In this study we investigated whether the enhanced arrest phenotype observed in Bcl-2 and Bcl-xL expressing cells is in part due to an enhanced autophagic response. During arrest conditions we treated cells with 3-methyladenine (3-MA), commonly used to inhibit autophagy, to determine whether Bcl-2 and Bcl-xL could still induce an enhanced arrest. We found that Bcl-xL expressing cells are not able to arrest effectively in G0 in the presence of 3-MA. This finding did not appear to be true for Bcl-2. These studies suggest that Bcl-xL mediates enhanced arrest in part through autophagy.
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| Files |
| Filename |
Size |
Approximate Download Time
(Hours:Minutes:Seconds)
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| 28.8 Modem |
56K Modem |
ISDN (64 Kb) |
ISDN (128 Kb) |
Higher-speed Access |
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Thesis.pdf.pdf |
542.70 Kb |
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