Title : Selective targeting of c-Abl via a cryptic mitochondrial targeting signal activated by cellular redox status in leukemic and breast cancer cells.

Pub. Date : 2012 Aug

PMID : 22549737






5 Functional Relationships(s)
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1 Fusing c-Abl to a mitochondrial translocation signal (MTS) that is activated by reactive oxygen species (ROS) will selectively target the mitochondria of cancer cells exhibiting an elevated ROS phenotype. Reactive Oxygen Species ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
2 Fusing c-Abl to a mitochondrial translocation signal (MTS) that is activated by reactive oxygen species (ROS) will selectively target the mitochondria of cancer cells exhibiting an elevated ROS phenotype. Reactive Oxygen Species ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
3 Fusing c-Abl to a mitochondrial translocation signal (MTS) that is activated by reactive oxygen species (ROS) will selectively target the mitochondria of cancer cells exhibiting an elevated ROS phenotype. Reactive Oxygen Species ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
4 METHODS: Confocal microscopy was used to determine mitochondrial colocalization of ectopically expressed c-Abl-EGFP/cMTS fusion across three cell lines (K562, Cos-7, and 1471.1) with varying levels of basal (and pharmacologically modulated) ROS. Reactive Oxygen Species ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
5 RESULTS: The cMTS and cMTS/c-Abl fusions colocalized to the mitochondria in leukemic (K562) and breast (1471.1) cancer phenotypes (but not Cos-7 fibroblasts) in a ROS and PKC dependent manner. Reactive Oxygen Species ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens