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dc.contributor.authorKang, J.
dc.contributor.authorPervaiz, Shazib
dc.identifier.citationKang, J. and Pervaiz, S. 2013. Crosstalk between Bcl-2 family and Ras family small GTPases: potential cell fate regulation?. Frontiers in Oncology. 2 JAN.

Cell fate regulation is a function of diverse cell signaling pathways that promote cell survival and or inhibit cell death execution. In this regard, the role of the Bcl-2 family in maintaining a tight balance between cell death and cell proliferation has been extensively studied. The conventional dogma links cell fate regulation by the Bcl-2 family to its effect on mitochondrial permeabilization and apoptosis amplification. However, recent evidence provide a novel mechanism for death regulation by the Bcl-2 family via modulating cellular redox metabolism. For example overexpression of Bcl-2 has been shown to contribute to a pro-oxidant intracellular milieu and down-regulation of cellular superoxide levels enhanced death sensitivity of Bcl-2 overexpressing cells. Interestingly, gene knockdown of the small GTPase Rac1 or pharmacological inhibition of its activity also reverted death phenotype in Bcl-2 expressing cells. This appears to be a function of an interaction between Bcl-2 and Rac1. Similar functional associations have been described between the Bcl-2 family and other members of the Ras superfamily. These interactions at the mitochondria provide novel opportunities for strategic therapeutic targeting of drug-resistant cancers. © 2013 Kang and Pervaiz.

dc.publisherFrontiers Research Foundation
dc.titleCrosstalk between Bcl-2 family and Ras family small GTPases: potential cell fate regulation?
dc.typeJournal Article
dcterms.source.volume2 JAN
dcterms.source.titleFrontiers in Oncology
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusOpen access via publisher

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