We have cloned the cDNA of the NDUFS5 subunit (15 kDa) of the human mitochondrial respiratory chain complex NADH: ubiquinone oxidoreductase (complex I). The open reading frame consists of 321 base-pairs, coding for 106 amino acids, with a calculated molecular mass of 12.5 kDa. There is an 81.0% identity with the bovine equivalent on cDNA level and 74.5% identity on amino acid basis. PCR analysis of rodent-human somatic cell hybrids revealed that the human NDUFS5 gene maps to chromosome 1. The NDUFS5 mRNA is expressed ubiquitously in human tissues, with a relative higher expression in human heart, skeletal muscle, liver, kidney and fetal heart. A mutation detection study of twenty isolated enzymatic complex I-deficient patients revealed no mutations, nor polymorphisms.
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http://dx.doi.org/10.1023/a:1005434912463 | DOI Listing |
Front Neurosci
January 2025
Department of Geriatric Rehabilitation, Jiangbin Hospital, Nanning, China.
Background: Programmed cell death plays an important role in neuronal injury and death after ischemic stroke (IS), leading to cellular glucose deficiency. Glucose deficiency can cause abnormal accumulation of cytotoxic disulfides, resulting in disulfidptosis. Ferroptosis, apoptosis, necroptosis, and autophagy inhibitors cannot inhibit this novel programmed cell death mechanism.
View Article and Find Full Text PDFMol Oncol
January 2025
Division of Cancer Cell Biology, Department of Pharmaceutical Sciences, Showa University Graduate School of Pharmacy, Tokyo, Japan.
The role of the electron transport chain (ETC) in cell proliferation control beyond its crucial function in supporting ATP generation has recently emerged. In this study, we found that, among the four ETC complexes, the complex I (CI)-mediated NAD regeneration is important for cancer cell proliferation. In cancer cells, a decrease in CI activity by RNA interference (RNAi) against NADH:ubiquinone oxidoreductase core subunit V1 (NDUFV1) arrested the cell cycle at the G/S phase, accompanying upregulation of p21 cyclin-dependent kinase inhibitor expression.
View Article and Find Full Text PDFBackground: Atherosclerosis (AS) is caused by the endothelium injury associated with oxidative stress. Previous studies have shown that the Phlegm-Eliminating and Stasis- Transforming Decoction (Huayu Qutan Decoction, HYQTD) has mitochondrial protective function. The objective of this research was to explore how HYQTD drug-containing serum (HYQTD-DS) could potentially protect mitochondrial energy production in endothelial cells (ECs) from injury caused by hydrogen peroxide (H2O2)-induced oxidative damage in AS through SIRT1/PGC-1α/ Nrf2 pathway.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
State Key Laboratory of Green Pesticide, International Joint Research Center for Intelligent Biosensor Technology and Health, Central China Normal University, Wuhan 430079, PR China. Electronic address:
Glyceraldehyde-3-phosphate dehydrogenase 2 (GAPDH2) plays a vital role in cell growth, stress responses, and various cellular processes in organisms. However, its functional characterization in cyanobacteria, particularly in Synechocystis sp. PCC 6803, remains largely unexplored, especially concerning its overexpression and RNA interference (RNAi) via double-stranded RNA (dsRNA).
View Article and Find Full Text PDFJ Child Neurol
January 2025
Department of Pediatrics, Division of Child Neurology, Ankara Etlik City Hospital, Ankara, Turkey.
Mitochondrial complex I transfers electrons from NADH (nicotinamide adenine dinucleotide) to ubiquinone, facilitating ATP synthesis via a proton gradient. Complex I defects are common among the mitochondrial diseases, especially in childhood. , located in complex I's transmembrane domain, is not directly involved in catalytic activity, but the mutations are associated with Leigh syndrome and complex I defects.
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