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Related Concept Videos

Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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ATP Synthase: Mechanism

In animals, the mitochondrial F1F0 ATP synthase is the key protein that synthesizes ATP molecules through a complex catalytic mechanism. While the nuclear genome encodes the majority of ATP synthase subunits, the mitochondrial genome encodes some of the enzyme's most critical components. The formation of this multi-subunit enzyme is a complex multi-step process regulated at the level of transcription, translation, and assembly. Defects in one or more of these steps can result in decreased ATP...
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The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...

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Related Experiment Video

Updated: Jul 7, 2026

Analyzing Supercomplexes of the Mitochondrial Electron Transport Chain with Native Electrophoresis, In-gel Assays, and Electroelution
08:37

Analyzing Supercomplexes of the Mitochondrial Electron Transport Chain with Native Electrophoresis, In-gel Assays, and Electroelution

Published on: June 1, 2017

Large-scale chemical dissection of mitochondrial function.

Bridget K Wagner1, Toshimori Kitami, Tamara J Gilbert

  • 1Broad Institute of Massachusetts Institute of Technology and Harvard, Seven Cambridge Center, Cambridge, Massachusetts 02142, USA.

Nature Biotechnology
|February 26, 2008
PubMed
Summary
This summary is machine-generated.

This study reveals how small molecules impact mitochondrial energy production (OXPHOS). It identifies drug combinations causing toxicity and others that may treat age-related diseases by regulating mitochondrial gene expression.

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Isolation of Mitochondria for Mitochondrial Supercomplex Analysis from Small Tissue and Cell Culture Samples
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Last Updated: Jul 7, 2026

Analyzing Supercomplexes of the Mitochondrial Electron Transport Chain with Native Electrophoresis, In-gel Assays, and Electroelution
08:37

Analyzing Supercomplexes of the Mitochondrial Electron Transport Chain with Native Electrophoresis, In-gel Assays, and Electroelution

Published on: June 1, 2017

Isolation of Mitochondria for Mitochondrial Supercomplex Analysis from Small Tissue and Cell Culture Samples
05:45

Isolation of Mitochondria for Mitochondrial Supercomplex Analysis from Small Tissue and Cell Culture Samples

Published on: May 3, 2024

Area of Science:

  • Cellular Biology
  • Biochemistry
  • Pharmacology

Background:

  • Mitochondrial oxidative phosphorylation (OXPHOS) is crucial for cellular energy homeostasis.
  • OXPHOS function is regulated by both mitochondrial (mtDNA) and nuclear genomes.
  • Understanding this integrated regulation is key to cellular function and disease.

Purpose of the Study:

  • To investigate the integrated regulation of OXPHOS function and physiology within cells.
  • To systematically map the effects of small-molecule perturbations on OXPHOS.
  • To identify novel therapeutic targets and understand drug-induced mitochondrial toxicity.

Main Methods:

  • Utilized four cell-based assays measuring OXPHOS physiology.
  • Performed multiplexed measurements of nuclear and mtDNA gene expression.
  • Screened 2,490 small-molecule perturbations in cultured muscle cells.

Main Results:

  • Protein synthesis inhibitors disrupted coordination between nuclear and mtDNA transcription.
  • Certain HMG-CoA reductase inhibitors with propranolol induced mitochondrial toxicity, offering insights into statin myopathy.
  • Microtubule inhibitors promoted OXPHOS transcription and reduced reactive oxygen species via PGC-1alpha and ERRalpha.

Conclusions:

  • The developed screening compendium is a valuable resource for studying mitochondrial biology and toxicity.
  • Identified potential therapeutic strategies for age-associated degenerative disorders using microtubule inhibitors.
  • Provided new understanding into the mechanisms of drug-induced mitochondrial dysfunction.