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

WRN Controls Formation of Extrachromosomal Telomeric Circles and Is Required for TRF2<sup>ΔB</sup>-Mediated Telomere Shortening

23 Jan 2008

Abstract excerpt

Telomere dysfunction has been proposed to contribute to the pathogenesis of Werner syndrome (WS), a premature-aging disorder. The WS protein WRN binds TRF2, a telomere-specific factor that protects chromosome ends. TRF2 possesses an amino-terminal domain that plays an essential role in preventing telomere shortening, as expression of TRF2(DeltaB), which lacks this domain, leads to the formation of telomeric...

Read the complete abstract on PubMed

Topics

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

Share to Chromosomal and Genetic Variations
Share to DNA Repair Mechanisms
Share to Telomeres, Telomerase, and Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 18212065
DOI: 10.1128/mcb.01364-07

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

WRN Controls Formation of Extrachromosomal Telomeric Circles and Is Required for TRF2<sup>ΔB</sup>-Mediated Telomere ShorteningPMID 18212065Read ↗

Telomeric protein TRF2 protects Holliday junctions with telomeric arms from displacement by the Werner syndrome helicaseSemantic proximity Read ↗

Telomere-binding Protein TRF2 Binds to and Stimulates the Werner and Bloom Syndrome HelicasesSemantic proximity Read ↗

Werner syndrome protein suppresses the formation of large deletions during the replication of human telomeric sequencesSemantic proximity Read ↗

Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome ProteinSemantic proximity Read ↗

WRN is recruited to damaged telomeres via its RQC domain and tankyrase1-mediated poly-ADP-ribosylation of TRF1Semantic proximity Read ↗

WRN regulates pathway choice between classical and alternative non-homologous end joiningSemantic proximity Read ↗

WRN, the protein deficient in Werner syndrome, plays a critical structural role in optimizing DNA repair.Semantic proximity Read ↗

Telomere dysfunction as a cause of genomic instability in Werner syndromeSemantic proximity Read ↗

TRF2 recruits the Werner syndrome (WRN) exonuclease for processing of telomeric DNASemantic proximity Read ↗

Defective telomere lagging strand synthesis in cells lacking WRN helicase activity.Semantic proximity Read ↗

Telomere shortening exposes functions for the mouse Werner and Bloom syndrome genes.Semantic proximity Read ↗

WRN as a Novel Target of Synthetic Lethality: Current Advances and Future PerspectivesSemantic proximity Read ↗

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