dc.creator | Valentin-Santiago, Mayda | |
dc.date.accessioned | 2020-08-22T00:14:51Z | |
dc.date.available | 2008-04-14 | |
dc.date.issued | 2007-04-14 | |
dc.identifier.uri | https://etd.library.vanderbilt.edu/etd-03302007-143206 | |
dc.identifier.uri | http://hdl.handle.net/1803/11732 | |
dc.description.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. | |
dc.format.mimetype | application/pdf | |
dc.subject | Bcl-xL | |
dc.subject | cell cycle | |
dc.subject | autophagy | |
dc.subject | Bcl-2 | |
dc.subject | Apoptosis -- Molecular aspects | |
dc.title | Role of Autophagy in BCL-2/BCL-XL Mediated G0 Arrest | |
dc.type | thesis | |
dc.contributor.committeeMember | Pran Datta | |
dc.type.material | text | |
thesis.degree.name | MS | |
thesis.degree.level | thesis | |
thesis.degree.discipline | Cancer Biology | |
thesis.degree.grantor | Vanderbilt University | |
local.embargo.terms | 2008-04-14 | |
local.embargo.lift | 2008-04-14 | |
dc.contributor.committeeChair | Elizabeth Yang | |