Evidence map›Paper›PMID 23685483›Full record

ArticleJournal of visualized experiments : JoVE2013

F1FO ATPase vesicle preparation and technique for performing patch clamp recordings of submitochondrial vesicle membranes.

Silvio Sacchetti, Kambiz N Alavian, Emma Lazrove, Elizabeth A Jonas

Open access · bronzeAbstract readVideo-Audio Media
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Mitochondrial Supercomplex-Associated Proximity Increases in Malignant Glioma Tissue.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Silvio SacchettiDepartment of Internal Medicine, Yale University, USA. silvio.sacchetti@yale.edu
Kambiz N Alavian
Emma Lazrove
Elizabeth A Jonas
Yale University · US

Funding

Mitochondrial Ion Channels in Hypoxic NeuronsR37NS045876 · NINDS · YALE UNIVERSITY · PI Elizabeth Ann Jonas · 2014 to 2026
$4.9M
Mitochondrial ion channels in hypoxic neuronsR01NS045876 · NINDS · YALE UNIVERSITY · PI JONAS, ELIZABETH ANN · 2004 to 2013
$3.3M
Role of BCL-xL in synaptic plasticity in the hippocampusR01NS064967 · NINDS · YALE UNIVERSITY · PI JONAS, ELIZABETH ANN · 2009 to 2010
$870k
Role of Bcl-xl in synaptic plasticity in the hippocampusR56NS064967 · NINDS · YALE UNIVERSITY · PI JONAS, ELIZABETH ANN · 2012 to 2012
$385k
NINDS NIH HHS R01 NS045876NINDS NIH HHS R01 NS064967NINDS NIH HHS R37 NS045876NINDS NIH HHS R56 NS064967
6 · The paper itself

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.

Indexed as

Adenosine TriphosphateAnimalsBlotting, WesternBrainMembrane Potential, MitochondrialMitochondriaMitochondrial MembranesPatch-Clamp TechniquesProton-Translocating ATPasesRatsAdenosine TriphosphateProton-Translocating ATPases

Identifiers

PMID23685483
PMCPMC3676267
OpenAlexW2059965813

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.