Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/35503
Title: THE SMALL GTPASE RAC1 IS A NOVEL BINDING PARTNER OF BCL-2 AND STABILIZES ITS ANTI-APOPTOTIC ACTIVITY
Authors: KANG JIA
Keywords: Rac1, Bcl-2, Apoptosis, ROS, Cancer, Interaction
Issue Date: 16-Jul-2012
Source: KANG JIA (2012-07-16). THE SMALL GTPASE RAC1 IS A NOVEL BINDING PARTNER OF BCL-2 AND STABILIZES ITS ANTI-APOPTOTIC ACTIVITY. ScholarBank@NUS Repository.
Abstract: We showed in this thesis that elevated superoxide levels at mitochondria are mediated through Rac1 activation induced by Bcl-2 overexpression in chronic myeloid leukaemia cell line model. We also demonstrated a physical interaction between Rac1 and Bcl-2 at the mitochondrial membranes. Disruption of the interaction led to a remarkable decrease in superoxide levels and sensitized the Bcl-2-overexpressing cancer cells to routine chemotherapeutic agents in chronic myeloid leukaemia and cervical cancer models, indicating that this interaction is contributing towards Bcl-2-mediated pro-oxidant state and chemoresistance. Further assessment on the functional relevance of this interaction through computer simulation in collaboration with ¿CELLWORKS Group Inc., identified STAT3 to positively correlate with the expression levels of Rac1 and Bcl-2. Subsequent wet lab experiments identified that STAT3 activation could be induced by Bcl-2-overexpression, which was mediated through Rac1 activation and superoxide production, suggesting that STAT3 activation could be a functional readout for Rac1-Bcl-2 interaction.
URI: http://scholarbank.nus.edu.sg/handle/10635/35503
Appears in Collections:Ph.D Theses (Open)

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
KangJ.pdf6.23 MBAdobe PDF

OPEN

NoneView/Download

Page view(s)

189
checked on Dec 11, 2017

Download(s)

50
checked on Dec 11, 2017

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.