CopA3 peptide from Copris tripartitus induces apoptosis in human Leukemia cells via a caspase-independent pathway
Our previous study demonstrated that CopA3, a disulfide dimer of the coprisin peptide analogue (LLCIALRKK), has antibacterial activity. In this study, we assessed whether CopA3 caused cellular toxicity in various mammalian cell lines. CopA3 selectively caused a marked decrease in cell viability in J...
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Published in | BMB reports Vol. 45; no. 2; pp. 85 - 90 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | Korean |
Published |
생화학분자생물학회
29.02.2012
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Subjects | |
Online Access | Get full text |
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Summary: | Our previous study demonstrated that CopA3, a disulfide dimer of the coprisin peptide analogue (LLCIALRKK), has antibacterial activity. In this study, we assessed whether CopA3 caused cellular toxicity in various mammalian cell lines. CopA3 selectively caused a marked decrease in cell viability in Jurkat T, U937, and AML-2 cells (human leukemia cells), but was not cytotoxic to Caki or Hela cells. Fragmentation of DNA, a marker of apoptosis, was also confirmed in the leukemia cell lines, but not in the other cells. CopA3-induced apoptosis in leukemia cells was mediated by apoptosis inducing factor (AIF), indicating induction of a caspase-independent signaling pathway. [BMB reports 2012; 45(2): 85-90]. |
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Bibliography: | Korean Society for Biochemistry and Molecular Biology KISTI1.1003/JNL.JAKO201208636393954 |
ISSN: | 1976-6696 1976-670X |