ArticleMolecular biology of the cell2002
Grx5 is a mitochondrial glutaredoxin required for the activity of iron/sulfur enzymes.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers.
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Who cites it
181 citing papers in PubMed, 454 citations in OpenAlex.
- Loss of TGME49_227100 (Glutaredoxin 5) Disrupts Oocyst Formation and Sporulation inPathogens (Basel, Switzerland) · 2026Article
- Monothiol glutaredoxins in microbial iron metabolism: From iron-sulfur cluster trafficking to iron-dependent regulation.Advances in microbial physiology · 2026Review
- The cytochrome oxidase defect in ISC-depleted yeast is caused by impaired iron-sulfur cluster maturation of the mitoribosome assembly factor Rsm22.FEBS letters · 2025Article
- Deficits in mitochondrial dynamics and iron balance result in templated insertions.Nature communications · 2025Article
- The thioredoxin-like and one glutaredoxin domain are required to rescue the iron-starvation phenotype of HeLa GLRX3 knock out cells.FEBS letters · 2025Article
- Redox-inactive CC-type glutaredoxins interfere with TGA transcription factor-dependent repression of target promoters in roots.The Plant cell · 2025Article
- Impact of Oxygen Availability on the Organelle-Specific Redox Potentials and Stress in Recombinant Protein Producing Komagataella phaffii.Microbial biotechnology · 2025Article
- Molecular basis for the enzymatic inactivity of class III glutaredoxin ROXY9 on standard glutathionylated substrates.Nature communications · 2025Article
- Isa2p is essential inJournal of biosciences · 2025Article
- Converging Roles of the Metal Transporter SMF11 and the Ferric Reductase FRE1 in Iron Homeostasis of Candida albicans.Molecular microbiology · 2024Article
- Auxotrophy-based curation improves the consensus genome-scale metabolic model of yeast.Synthetic and systems biotechnology · 2024Article
- Characterizing age-related changes in intact mitochondrial proteoforms in murine hearts using quantitative top-down proteomics.Clinical proteomics · 2024Article
- Mitochondria function in cytoplasmic FeS protein biogenesis.Biochimica et biophysica acta. Molecular cell research · 2024Review
- Capsicum chinense Jacq.-derived glutaredoxin (CcGRXS12) alters redox status of the cells to confer resistance against pepper mild mottle virus (PMMoV-I).Plant cell reports · 2024Article
- Mitochondrial Glutathione in Cellular Redox Homeostasis and Disease Manifestation.International journal of molecular sciences · 2024Review
- The Monothiol Glutaredoxin Grx4 Influences Iron Homeostasis and Virulence inJournal of fungi (Basel, Switzerland) · 2023Article
- Adaptation of the late ISC pathway in the anaerobic mitochondrial organelles of Giardia intestinalis.PLoS pathogens · 2023Article
- New Perspectives on BolA: A Still Mysterious Protein Connecting Morphogenesis, Biofilm Production, Virulence, Iron Metabolism, and Stress Survival.Microorganisms · 2023Review
- Regulation of Mitochondrial Energy Metabolism by Glutaredoxin 5 in the Apicomplexan Parasite Neospora caninum.Microbiology spectrum · 2023Article
- Monothiol Glutaredoxin Is Essential for Oxidative Stress Protection and Virulence in Pseudomonas aeruginosa.Applied and environmental microbiology · 2023Article
121 more citing papers are in PubMed but not listed here.
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Yeast cells contain a family of three monothiol glutaredoxins: Grx3, 4, and 5. Absence of Grx5 leads to constitutive oxidative damage, exacerbating that caused by external oxidants. Phenotypic defects associated with the absence of Grx5 are suppressed by overexpression of SSQ1 and ISA2, two genes involved in the synthesis and assembly of iron/sulfur clusters into proteins. Grx5 localizes at the mitochondrial matrix, like other proteins involved in the synthesis of these clusters, and the mature form lacks the first 29 amino acids of the translation product. Absence of Grx5 causes: 1) iron accumulation in the cell, which in turn could promote oxidative damage, and 2) inactivation of enzymes requiring iron/sulfur clusters for their activity. Reduction of iron levels in grx5 null mutants does not restore the activity of iron/sulfur enzymes, and cell growth defects are not suppressed in anaerobiosis or in the presence of disulfide reductants. Hence, Grx5 forms part of the mitochondrial machinery involved in the synthesis and assembly of iron/sulfur centers.
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