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Title page for ETD etd-03302007-143206


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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