Abstract
Background: Surface expression of complement inhibitors, such as the glycosylphosphatidylinositol-anchored protein CD59, prevent complement-dependent lysis of cancer cells. Results: The non-toxic domain-4 of the bacterial toxin intermedilysin (rILYd4) blocks CD59 complement inhibitory activity. Conclusion: rILYd4 induces CD59 internalization and rapid degradation in lysosomes in non-small lung carcinoma cells. Significance: CD59 serves as a model for glycosylphosphatidylinositol-anchored protein trafficking and rILYd4 shows potential for immunotherapy.
Original language | English |
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Pages (from-to) | 12109-12125 |
Number of pages | 17 |
Journal | Journal of Biological Chemistry |
Volume | 289 |
Issue number | 17 |
DOIs | |
State | Published - 25 Apr 2014 |
Externally published | Yes |