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

Effects of deleting mitochondrial antioxidant genes on life span.

Annals of the New York Academy of Sciences - 1 Apr 2007

Unlu Ercan Selcuk, Koc Ahmet

Abstract excerpt

Reactive oxygen species (ROS) damage biomolecules, accelerate aging, and shorten life span, whereas antioxidant enzymes mitigate these effects. Because mitochondria are a primary site of ROS generation and also a primary target of ROS attack, they have become a major focus area of aging studies. Here, we employed yeast genetics to identify mitochondrial antioxidant genes that are important for replicative life...

Read the complete abstract on PubMed

Topics

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

Share to Antioxidants
Share to Cellular Senescence
Share to Gene Expression Regulation, Fungal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genes, Fungal

Share to Genes, Mitochondrial

Share to Oxidative Stress

Share to Reactive Oxygen Species

Share to Superoxide Dismutase

Source

Identifiers

PMID: 17460215
DOI: 10.1196/annals.1395.055

Genes

SOD1
SOD2

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

Effects of deleting mitochondrial antioxidant genes on life span.PMID 17460215Read ↗

Absence of superoxide dismutase activity causes nuclear DNA fragmentation during the aging process.Semantic proximity Read ↗

Mitochondrial Efficiency-Dependent Viability of Saccharomyces cerevisiae Mutants Carrying Individual Electron Transport Chain Component Deletions.Semantic proximity Read ↗

The role of thioredoxin in the aging process: involvement of oxidative stress.Semantic proximity Read ↗

Overexpressed Sod1p acts either to reduce or to increase the lifespans and stress resistance of yeast, depending on whether it is Cu(2+)-deficient or an active Cu,Zn-superoxide dismutase.Semantic proximity Read ↗

Effects of the mitochondrial respiratory chain on longevity in C. elegans.Semantic proximity Read ↗

SOD2 functions downstream of Sch9 to extend longevity in yeast.Semantic proximity Read ↗

The effects of catalase gene overexpression on life span and resistance to oxidative stress in transgenic Drosophila melanogasterSemantic proximity Read ↗

A Measurable increase in oxidative damage due to reduction in superoxide detoxification fails to shorten the life span of long-lived mitochondrial mutants of Caenorhabditis elegans.Semantic proximity Read ↗

The roles of thiol oxidoreductases in yeast replicative aging.Semantic proximity Read ↗

Copper supplementation increases yeast life span under conditions requiring respiratory metabolism.Semantic proximity Read ↗

Requirement of glutathione for Sod1 activation during lifespan extension.Semantic proximity Read ↗

Extending life span by increasing oxidative stressSemantic proximity Read ↗

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