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Atypical protein kinase C in cell motility

期刊

CELLULAR AND MOLECULAR LIFE SCIENCES
卷 70, 期 17, 页码 3057-3066

出版社

SPRINGER BASEL AG
DOI: 10.1007/s00018-012-1192-1

关键词

Cell migration; Cell invasion; Podosome; Invadopodia; Lamellipodia; MMP

资金

  1. Canadian Institutes of Health Research (CIHR) [MOP-13270, MOP-42 546, MOP-119514]
  2. Peterborough K.M. Hunter Graduate Studentship for Cancer Research

向作者/读者索取更多资源

Cell motility is defined as cell movement in the three-dimensional space leading to repositioning of the cell. Atypical protein kinase C (aPKC, including zeta and lambda/iota) are a subfamily of PKC. Different from classic PKC and novel PKC, the activation of atypical PKC is not dependent on diacylglycerol or calcium. PKC zeta 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 PKC zeta. 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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