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Atypical protein kinase C in cell motility |
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| Authors: | Helan Xiao Mingyao Liu |
| Institution: | 1. Latner Thoracic Surgery Research Laboratories, Toronto General Research Institute, University Health Network, Toronto, ON, Canada 2. Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada 3. Department of Surgery and Medicine, Faculty of Medicine, University of Toronto, Toronto, ON, Canada 4. Institute of Medical Science, Faculty of Medicine, University of Toronto, Toronto, ON, Canada 5. Faculty of Medicine, University of Toronto, Toronto General Hospital, Room TMDT 2-814, 101 College Street, Toronto, ON, M5G 1L7, Canada |
| Abstract: | Cell motility is defined as cell movement in the three-dimensional space leading to repositioning of the cell. Atypical protein kinase C (aPKC, including ζ and λ/ι) are a subfamily of PKC. Different from classic PKC and novel PKC, the activation of atypical PKC is not dependent on diacylglycerol or calcium. PKCζ can be activated by lipid components, such as phosphatidylinositols, phosphatidic acid, arachidonic acid, and ceramide. Both phosphatidylinositol (3,4,5)-trisphosphate and PDK1 are necessary for the complete and stable activation of PKCζ. Atypical PKC is involved in the regulation of cell polarization, directional sensing, formation of filopodia, and cell motility. It is essential for migration and invasion of multiple cancer cell types. Particularly, atypical PKC has been found in the regulation of the motility of hematopoietic cells. It also participates in the regulation of proteolytic activity of podosomes and invadopodia. It has been found that atypical PKC can work coordinately with other PKC subfamily members and other signaling pathways. Research on the roles of atypical PKC in cell motility may lead to new therapeutic strategies for cancer and other diseases. |
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