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Role of Autophagy in BCL-2/BCL-XL Mediated G0 Arrest

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.

Identiferoai:union.ndltd.org:VANDERBILT/oai:VANDERBILTETD:etd-03302007-143206
Date14 April 2007
CreatorsValentin-Santiago, Mayda
ContributorsPran Datta, Elizabeth Yang
PublisherVANDERBILT
Source SetsVanderbilt University Theses
LanguageEnglish
Detected LanguageEnglish
Typetext
Formatapplication/pdf
Sourcehttp://etd.library.vanderbilt.edu/available/etd-03302007-143206/
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