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

Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.

Nucleic acids research - 18 Sept 2015

Muraki Keiko, Han Limei, Miller Douglas, Murnane John P

Abstract excerpt

The caps on the ends of chromosomes, called telomeres, keep the ends of chromosomes from appearing as DNA double-strand breaks (DSBs) and prevent chromosome fusion. However, subtelomeric regions are sensitive to DSBs, which in normal cells is responsible for ionizing radiation-induced cell senescence and protection against oncogene-induced replication stress, but promotes chromosome instability in cancer cells...

Read the complete abstract on PubMed

Topics

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

Share to Chromosome Aberrations
Share to DNA Breaks, Double-Stranded

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA End-Joining Repair

Share to Exodeoxyribonucleases

Share to MRE11 Homologue Protein

Share to Pyrimidinones

Share to Sequence Deletion

Share to Telomere

Source

Open in PubMed Open full text

Identifiers

PMID: 26209132
DOI: 10.1093/nar/gkv714
PMCID: PMC4652756

Genes

MRE11

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

Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.PMID 26209132Read ↗

Exonuclease function of human Mre11 promotes deletional nonhomologous end joining.Semantic proximity Read ↗

Role of Mre11 in chromosomal nonhomologous end joining in mammalian cells.Semantic proximity Read ↗

DNA End Resection: Facts and MechanismsSemantic proximity Read ↗

The high toxicity of DSB-clusters modelling high-LET-DNA damage derives from inhibition of c-NHEJ and promotion of alt-EJ and SSA despite increases in HRSemantic proximity Read ↗

DNA double-strand break end resection: a critical relay point for determining the pathway of repair and signalingSemantic proximity Read ↗

The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosisSemantic proximity Read ↗

DNA end resection is needed for the repair of complex lesions in G1-phase human cellsSemantic proximity Read ↗

Cas9-induced large deletions and small indels are controlled in a convergent fashionSemantic proximity Read ↗

Structurally distinct Mre11 domains mediate MRX functions in resection, end-tethering and DNA damage resistance.Semantic proximity Read ↗

ATM regulates Mre11-dependent DNA end-degradation and microhomology-mediated end joiningSemantic proximity Read ↗

Chromosome Instability as a Result of Double-Strand Breaks near Telomeres in Mouse Embryonic Stem CellsSemantic proximity Read ↗

Regulation of DNA Double Strand Breaks Processing: Focus on BarriersSemantic proximity Read ↗

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