ArticleJournal of visualized experiments : JoVE2013
F1FO ATPase vesicle preparation and technique for performing patch clamp recordings of submitochondrial vesicle membranes.
Article in Journal of visualized experiments : JoVE, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Mitochondrial Supercomplex-Associated Proximity Increases in Malignant Glioma Tissue.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Investigation of mitochondrial inner membrane ion conductance by planar lipid bilayer electrophysiology.Frontiers in physiology · 2026Article
- A mitochondrial megachannel resides in monomeric FNature communications · 2019Article
- Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicity.Cell death and differentiation · 2017Article
- The mitochondrial complex V-associated large-conductance inner membrane current is regulated by cyclosporine and dexpramipexole.Molecular pharmacology · 2015Article
- Did a classic preconditioning study provide a clue to the identity of the mitochondrial permeability transition pore?Circulation research · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are involved in many important cellular functions including metabolism, survival(1), development and, calcium signaling(2). Two of the most important mitochondrial functions are related to the efficient production of ATP, the energy currency of the cell, by oxidative phosphorylation, and the mediation of signals for programmed cell death(3). The enzyme primarily responsible for the production of ATP is the F1FO-ATP synthase, also called ATP synthase(4-5). In recent years, the role of mitochondria in apoptotic and necrotic cell death has received considerable attention. In apoptotic cell death, BCL-2 family proteins such as Bax enter the mitochondrial outer membrane, oligomerize and permeabilize the outer membrane, releasing pro-apoptotic factors into the cytosol(6). In classic necrotic cell death, such as that produced by ischemia or excitotoxicity in neurons, a large, poorly regulated increase in matrix calcium contributes to the opening of an inner membrane pore, the mitochondrial permeability transition pore or mPTP. This depolarizes the inner membrane and causes osmotic shifts, contributing to outer membrane rupture, release of pro-apoptotic factors, and metabolic dysfunction. Many proteins including Bcl-xL(7) interact with F1FO ATP synthase, modulating its function. Bcl-xL interacts directly with the beta subunit of F1FO ATP synthase, and this interaction decreases a leak conductance within the F1FOATPasecomplex, increasing the net transport of H+ by F1FO during F1FO ATPase activity(8) and thereby increasing mitochondrial efficiency. To study the activity and modulation of the ATP synthase, we isolated from rodent brain submitochondrial vesicles (SMVs) containing F1FO ATPase. The SMVs retain the structural and functional integrity of the F1FO ATPase as shown in Alavian et al. Here, we describe a method that we have used successfully for the isolation of SMVs from rat brain and we delineate the patch clamp technique to analyze channel activity (ion leak conductance) of the SMVs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.