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

Congenital DNA repair deficiency results in protection against renal ischemia reperfusion injury in mice.

Aging cell - 1 Apr 2009

Susa Denis, Mitchell James R, Verweij Marielle, van de Ven Marieke, Roest Henk, van den Engel Sandra, Bajema Ingeborg, Mangundap Kirsten, Ijzermans Jan N M, Hoeijmakers Jan H J, de Bruin Ron W F

Abstract excerpt

Cockayne syndrome and other segmental progerias with inborn defects in DNA repair mechanisms are thought to be due in part to hypersensitivity to endogenous oxidative DNA damage. The accelerated aging-like symptoms of this disorder include dysmyelination within the central nervous system, progressive sensineuronal hearing loss and retinal degeneration. We tested the effects of congenital nucleotide excision DNA...

Read the complete abstract on PubMed

Topics

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

Share to Cockayne Syndrome
Share to DNA Repair Enzymes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Glucose Tolerance Test

Share to Insulin Resistance

Share to Ischemia

Share to Poly-ADP-Ribose Binding Proteins

Share to Renal Insufficiency

Share to Reperfusion Injury

Source

Open in PubMed Open full text

Identifiers

PMID: 19338497
DOI: 10.1111/j.1474-9726.2009.00463.x
PMCID: PMC2701740

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

Congenital DNA repair deficiency results in protection against renal ischemia reperfusion injury in mice.PMID 19338497Read ↗

Repair of oxidatively generated DNA damage in Cockayne syndrome.Semantic proximity Read ↗

Cockayne syndrome pathogenesis: lessons from mouse models.Semantic proximity Read ↗

Dysmyelination not demyelination causes neurological symptoms in preweaned mice in a murine model of Cockayne syndrome.Semantic proximity Read ↗

Cockayne syndrome group B (Csb) and group a (Csa) deficiencies predispose to hearing loss and cochlear hair cell degeneration in mice.Semantic proximity Read ↗

Increased apoptosis, p53 up-regulation, and cerebellar neuronal degeneration in repair-deficient Cockayne syndrome miceSemantic proximity Read ↗

Loss of genome maintenance accelerates podocyte damage and agingSemantic proximity Read ↗

Cockayne syndrome mice reflect human kidney disease and are defective in de novo NAD biosynthesisSemantic proximity Read ↗

Loss of genome maintenance is linked to mTOR complex 1 signaling and accelerates podocyte damageSemantic proximity Read ↗

Cell-Autonomous Progeroid Changes in Conditional Mouse Models for Repair Endonuclease XPG DeficiencySemantic proximity Read ↗

Mitochondrial and NAD+ metabolism predict recovery from acute kidney injury in a diverse mouse populationSemantic proximity Read ↗

[The metabolic and molecular bases of Cockayne syndrome].Semantic proximity Read ↗

p53 regulates diverse tissue-specific outcomes to endogenous DNA damage in miceSemantic proximity Read ↗

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