Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10765371 | Biochemical and Biophysical Research Communications | 2010 | 6 Pages |
Abstract
We prepared GD3-7-aldehyde (GD3-7) and determined its apoptotic potential. GD3-7 proved to be more efficient to induce pro-apoptotic mitochondrial alterations than GD3 when tested on mouse liver mitochondria. GD3-7-induced mitochondrial swelling and depolarization was blocked by cyclosporin A (CsA) supporting a critical role of the permeability transition pore complex (PTPC) during GD3-7-mediated apoptosis. In contrast to GD3, GD3-7 was able to induce channel formation in proteoliposomes containing adenine nucleotide translocase (ANT). This suggests that ANT is the molecular target of GD3-7. Using a specific antiserum, GD3-7 was detected in the lipid extract of the myeloid tumor cell line HL-60 after apoptosis induction, but not in living cells. Therefore, GD3-7 might be a novel mediator of PTPC-dependent apoptosis in cancer cells.
Keywords
MMPII3(NeuAc)2-LacCerII3NeuAc-LacCerCarboxyatractylosidePTPCCypDGM3GD3Cyclophilin DVDACΔΨmAMUANTCATCSAadenine nucleotide translocaseApoptosiscyclosporin Apermeability transition pore complexMitochondrial membrane permeabilizationatomic mass unitsMitochondrial transmembrane potentialvoltage-dependent anion channel
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Authors
Catherine Brenner, Bernhard Kniep, Evelyne Maillier, Cécile Martel, Claudia Franke, Nadja Röber, Michael Bachmann, Ernst Peter Rieber, Roger Sandhoff,