Abstract
MccJ25, an antimicrobial peptide, was unable to cause apoptosis of COS-7 cells in spite of inducing reactive-oxygen species overproduction as well as cytochrome c release from isolated mitochondria. Surprisingly, MccJ25-Ga, an amidated variant of MccJ25 that displays similar anti-mitochondrial effects, did induce apoptosis in COS-7. The only difference found between the activities of these peptides was the unpredicted inhibition of mitochondrial RNA synthesis by MccJ25-Ga. These results led us to hypothesize that both mitochondrial RNA polymerase and mitochondrial membrane might be the molecular targets of MccJ25-Ga in mitochondria and this combined effect may lead to apoptosis.
Original language | English |
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Pages (from-to) | 832-834 |
Number of pages | 3 |
Journal | Peptides |
Volume | 32 |
Issue number | 4 |
DOIs | |
Publication status | Published - Apr 2011 |
Funding
Financial support was provided by CONICET (Grant PIP 4996 ) and CIUNT (Grant 26/D228 ) and the Agencia Nacional de Promoción Científica y Técnica (PICTO 843, PAE 22642). M.V.N. and F.D. were recipient of a CONICET fellowship. R.D.M., C.M., L.S., E.H. and C.B. are career investigator of CONICET. We want to thank to Dr. Manuel Aybar and Dr. Tristán Agüero for their generous assistance.
Keywords
- Apoptosis
- Microcin
- Mitochondria
- RNA-polymerase
ASJC Scopus subject areas
- Biochemistry
- Physiology
- Endocrinology
- Cellular and Molecular Neuroscience