Abstract
Mitochondrial permeabilisation after NO donor application did not activate caspase-9. We have studied the X-linked apoptosis inhibitor (XIAP) and Aven protein content in NO-treated Jurkat cells. The level of both proteins increased in NO-treated cells. Thus the increase in XIAP and Aven content could be the cause of the lack of caspase-9 activity after mitochondrial permeabilisation in NO-treated Jurkat cells.
Keywords:
Aven; XIAP; apoptosis; caspase; mitochondria; nitric oxide.
© 2014 International Federation for Cell Biology.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / metabolism*
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Apoptosis / drug effects
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Apoptosis Regulatory Proteins / metabolism*
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Caspase 9 / metabolism
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Humans
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Jurkat Cells
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Membrane Potential, Mitochondrial / drug effects
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Membrane Proteins / metabolism*
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Mitochondria / drug effects*
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Mitochondria / metabolism
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Nitric Oxide Donors / pharmacology*
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Permeability / drug effects
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Triazenes / pharmacology*
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X-Linked Inhibitor of Apoptosis Protein / metabolism*
Substances
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1-hydroxy-2-oxo-3-(3-aminopropyl)-3-isopropyl-1-triazene
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AVEN protein, human
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Adaptor Proteins, Signal Transducing
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Apoptosis Regulatory Proteins
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Membrane Proteins
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Nitric Oxide Donors
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Triazenes
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X-Linked Inhibitor of Apoptosis Protein
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Caspase 9