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  • Bax does not directly participate in the Ca(2+)-induced permeability transition of isolated mitochondria.

Bax does not directly participate in the Ca(2+)-induced permeability transition of isolated mitochondria.

The Journal of biological chemistry (2004-07-02)
Umberto De Marchi, Silvia Campello, Ildikò Szabò, Francesco Tombola, Jean-Claude Martinou, Mario Zoratti
초록

The mitochondrial permeability transition pore and Bax have both been proposed to be involved in the release of pro-apoptotic factors from mitochondria in the "intrinsic" pathway of apoptosis. The permeability transition pore is widely thought to be a supramolecular complex including or interacting with Bax. Given the relevance of the permeability transition in vivo, we have verified whether Bax influences the formation and/or the properties of the Ca(2+)/P(i)-induced permeability transition by using mitochondriaisolated from isogenic human colon cancer bax(+/-) and bax(-/-) HCT116 cell lines. We used mitochondria isolated from both types of cells and from Bax(+) cells exposed to apoptotic stimuli, as well as Bax-less mitochondria into which exogenous Bax had been incorporated. All exhibited the same behavior and pharmacological profile in swelling and Ca(2+)-retention experiments. Mitochondria from a bax(-)/bak(-) cell line also underwent an analogous Ca(2+)/P(i)-inducible swelling. This similarity indicates that Bax hasno major role in regulating the Ca(2+)-induced mitochondrial permeability transition.

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Sigma-Aldrich
4-Ethylphenol, ≥97.0% (GC)
Sigma-Aldrich
Anti-Bak Antibody, NT, Upstate®, from rabbit