ArticleBiochimica et biophysica acta2014
ND3, ND1 and 39kDa subunits are more exposed in the de-active form of bovine mitochondrial complex I.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Potential for flexible lactate shuttling between astrocytes and neurons to mitigate against diving-induced hypoxia.Frontiers in neuroanatomy · 2025Article
- Translation Fidelity and Respiration Deficits in CLPP-Deficient Tissues: Mechanistic Insights from Mitochondrial Complexome Profiling.International journal of molecular sciences · 2023Article
- The coupling mechanism of mammalian mitochondrial complex I.Nature structural & molecular biology · 2022Article
- Accessory Subunits of the Matrix Arm of Mitochondrial Complex I with a Focus on Subunit NDUFS4 and Its Role in Complex I Function and Assembly.Life (Basel, Switzerland) · 2021Review
- Proteomic analysis reveals ginsenoside Rb1 attenuates myocardial ischemia/reperfusion injury through inhibiting ROS production from mitochondrial complex I.Theranostics · 2021Article
- Nitric Oxide in Macrophage Immunometabolism: Hiding in Plain Sight.Metabolites · 2020Review
- Brain Ischemia/Reperfusion Injury and Mitochondrial Complex I Damage.Biochemistry. Biokhimiia · 2019Review
- Article
- Exploring the quinone/inhibitor-binding pocket in mitochondrial respiratory complex I by chemical biology approaches.The Journal of biological chemistry · 2019Article
- Effect of Aging on Mitochondrial Energetics in the Human Atria.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
- Long-range proton-coupled electron transfer in biological energy conversion: towards mechanistic understanding of respiratory complex I.Journal of the Royal Society, Interface · 2018Review
- Structure of the Deactive State of Mammalian Respiratory Complex I.Structure (London, England : 1993) · 2018Article
- Clarifying the supercomplex: the higher-order organization of the mitochondrial electron transport chain.Nature structural & molecular biology · 2017Review
- Modulation of the conformational state of mitochondrial complex I as a target for therapeutic intervention.Interface focus · 2017Review
- Mitochondrial Dysfunction and Myocardial Ischemia-Reperfusion: Implications for Novel Therapies.Annual review of pharmacology and toxicology · 2017Review
- Activation of respiratory Complex I fromHeliyon · 2017Article
- A LON-ClpP Proteolytic Axis Degrades Complex I to Extinguish ROS Production in Depolarized Mitochondria.Cell reports · 2016Article
- Complex I assembly into supercomplexes determines differential mitochondrial ROS production in neurons and astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Structure of mammalian respiratory complex I.Nature · 2016Article
- Ischemic A/D transition of mitochondrial complex I and its role in ROS generation.Biochimica et biophysica acta · 2016Review
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Authors and funding
9 authors.
Funding
Abstract
An intriguing feature of mitochondrial complex I from several species is the so-called A/D transition, whereby the idle enzyme spontaneously converts from the active (A) form to the de-active (D) form. The A/D transition plays an important role in tissue response to the lack of oxygen and hypoxic deactivation of the enzyme is one of the key regulatory events that occur in mitochondria during ischaemia. We demonstrate for the first time that the A/D conformational change of complex I does not affect the macromolecular organisation of supercomplexes in vitro as revealed by two types of native electrophoresis. Cysteine 39 of the mitochondrially-encoded ND3 subunit is known to become exposed upon de-activation. Here we show that even if complex I is a constituent of the I+III2+IV (S1) supercomplex, cysteine 39 is accessible for chemical modification in only the D-form. Using lysine-specific fluorescent labelling and a DIGE-like approach we further identified two new subunits involved in structural rearrangements during the A/D transition: ND1 (MT-ND1) and 39kDa (NDUFA9). These results clearly show that structural rearrangements during de-activation of complex I include several subunits located at the junction between hydrophilic and hydrophobic domains, in the region of the quinone binding site. De-activation of mitochondrial complex I results in concerted structural rearrangement of membrane subunits which leads to the disruption of the sealed quinone chamber required for catalytic turnover.
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