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| Cancer Res. Mar (2003); 63(6):1153-6 | |
| Phospholipid scramblase 3 is the mitochondrial target of protein kinase C delta-induced apoptosis. | |
| Liu J, Chen J, Dai Q, Lee RM | |
| Huntsman Cancer Institute and Section of Oncology, Department of Medicine, University of Utah, Salt Lake City, Utah 84112, USA. | |
| Abstract: Protein kinase C (PKC) delta translocates to mitochondria during apo-ptosis,but its mitochondrial target remains unclear. We found that PKC-delta physically interacted with and phosphorylated phospholipid scramblase 3 (PLS3) after UV irradiation. PLS3 is a high-affinity substrate for PKC-delta in vitro with the K(m) at 10.5 nM. Cells expressing wild-type PLS3 became apoptotic on phorbol ester stimulation, whereas the control cells did not. Expression of a mitochondrial-targeted PKC-delta enhanced apoptosis more prominently in HeLa-PLS3 cells than control HeLa cells and HeLa cells expressing an inactive PLS3 mutant. These results indicate that PLS3 is a downstream effector of PKC-delta in the mitochondria. | |
| [PUBMED: 12649167] |   |
| Copyright © 2009, Tyers Lab, The Samuel Lunenfeld Research Institute, Mount Sinai Hospital, All Rights Reserved. |
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| BioGRID: A General Repository for Interaction Datasets. Chris Stark, Bobby-Joe Breitkreutz, Teresa Reguly, Lorrie Boucher, Ashton Breitkreutz, Mike Tyers. Nucleic Acids Res. Jan 1;34:D535-9. |