Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Restoration of mitochondrial function in cells with complex I deficiency.

Annals of the New York Academy of Sciences - 1 May 2005

Bai Yidong, Park Jeong Soon, Deng Jian-Hong, Li Youfen, Hu Peiqing

Abstract excerpt

The mammalian mitochondrial NADH dehydrogenase (complex I) is the major entry point for the electron transport chain. It is the largest and most complicated respiratory complex consisting of at least 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA). Deficiency in complex I function has been associated with various human diseases including neurodegenerative diseases and the aging process. To...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to DNA, Mitochondrial
Share to Electron Transport Complex I

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation

Share to Mitochondria

Share to Mutation

Share to Protein Subunits

Source

Identifiers

PMID: 15965042
DOI: 10.1196/annals.1338.003

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Restoration of mitochondrial function in cells with complex I deficiency.PMID 15965042Read ↗

Can a Single Subunit Yeast NADH Dehydrogenase (Ndi1) Remedy Diseases Caused by Respiratory Complex I Defects?Semantic proximity Read ↗

Respiratory chain complex I deficiency.Semantic proximity Read ↗

Mitochondrial complex I deficiency: from organelle dysfunction to clinical disease.Semantic proximity Read ↗

Mitochondrial disease associated with complex I (NADH-CoQ oxidoreductase) deficiency.Semantic proximity Read ↗

Current Options in the Treatment of Mitochondrial DiseasesSemantic proximity Read ↗

Cellular and animal models for mitochondrial complex I deficiency: a focus on the NDUFS4 subunit.Semantic proximity Read ↗

Preparation of respiratory chain complexes from Saccharomyces cerevisiae wild-type and mutant mitochondria : activity measurement and subunit composition analysis.Semantic proximity Read ↗

In vivo dissection of the mitochondrial respiratory NADH: ubiquinone oxidoreductase (complex I).Semantic proximity Read ↗

The NADH:ubiquinone oxidoreductase (complex I) of respiratory chains.Semantic proximity Read ↗

Pharmacological NAD-Boosting Strategies Improve Mitochondrial Homeostasis in Human Complex I-Mutant Fibroblasts.Semantic proximity Read ↗

NAD(+)-dependent activation of Sirt1 corrects the phenotype in a mouse model of mitochondrial disease.Semantic proximity Read ↗

[Complex I (NADH-ubiquinone oxidoreductase) deficiency].Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.