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

Meiotic resetting of the cellular Sod1 pool is driven by protein aggregation, degradation, and transient LUTI-mediated repression.

The Journal of cell biology - 6 Mar 2023

Vander Wende Helen M, Gopi Mounika, Onyundo Megan, Medrano Claudia, Adanlawo Temiloluwa, Brar Gloria Ann

Abstract excerpt

Gametogenesis requires packaging of the cellular components needed for the next generation. In budding yeast, this process includes degradation of many mitotically stable proteins, followed by their resynthesis. Here, we show that one such case-Superoxide dismutase 1 (Sod1), a protein that commonly aggregates in human ALS patients-is regulated by an integrated set of events, beginning with the formation of...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis
Share to Meiosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mutation

Share to Protein Aggregates

Share to Saccharomyces cerevisiae

Share to Saccharomyces cerevisiae Proteins

Share to Superoxide Dismutase-1

Share to Unfolded Protein Response

Source

Open in PubMed Open full text

Identifiers

PMID: 36622328
DOI: 10.1083/jcb.202206058
PMCID: PMC9836244

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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

Meiotic resetting of the cellular Sod1 pool is driven by protein aggregation, degradation, and transient LUTI-mediated repression.PMID 36622328Read ↗

Meiotic resetting of the cellular Sod1 pool is driven by protein aggregation, degradation, and transient LUTI-mediated repressionSemantic proximity Read ↗

Gametogenesis: Exploring an Endogenous Rejuvenation Program to Understand Cellular Aging and Quality ControlSemantic proximity Read ↗

SOD1 oxidation and formation of soluble aggregates in yeast: relevance to sporadic ALS development.Semantic proximity Read ↗

SOD1 Function and Its Implications for Amyotrophic Lateral Sclerosis Pathology: New and Renascent Themes.Semantic proximity Read ↗

Degradation-mediated protein quality control in the nucleus.Semantic proximity Read ↗

Factors controlling the uptake of yeast copper/zinc superoxide dismutase into mitochondria.Semantic proximity Read ↗

ALS-linked SOD1 mutations impair mitochondrial-derived vesicle formation and accelerate aging.Semantic proximity Read ↗

Mitochondrial quality control during inheritance is associated with lifespan and mother-daughter age asymmetry in budding yeast.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 ↗

Different regulation of wild-type and mutant Cu,Zn superoxide dismutase localization in mammalian mitochondria.Semantic proximity Read ↗

Import, maturation, and function of SOD1 and its copper chaperone CCS in the mitochondrial intermembrane space.Semantic proximity Read ↗

Posttranscriptional regulation of SOD1 gene expression under oxidative stress: Potential role of ELAV proteins in sporadic ALSSemantic proximity Read ↗

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