Rapid degradation of the complement regulator, CD59, by a novel inhibitor

Bishuang Cai, Shuwei Xie, Fengming Liu, Laura C. Simone, Steve Caplan, Xuebin Qin, Naava Naslavsky

Research output: Contribution to journalArticle

9 Scopus citations

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 languageEnglish (US)
Pages (from-to)12109-12125
Number of pages17
JournalJournal of Biological Chemistry
Volume289
Issue number17
DOIs
StatePublished - Apr 25 2014

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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