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

A postincision-deficient TFIIH causes replication fork breakage and uncovers alternative Rad51- or Pol32-mediated restart mechanisms.

Molecular cell - 12 Mar 2010

Moriel-Carretero María, Aguilera Andrés

Abstract excerpt

Homologous recombination is a major double-strand break (DSB) repair mechanism that acts during the S and G2 phases. In contrast, nucleotide excision repair (NER) is a major pathway for the repair of DNA bulky adducts that is unrelated to replication. We show that replication can be strongly disturbed in a specific type of rad3/XPD NER mutant of TFIIH, causing replication fork breakage. In contrast to classical...

Read the complete abstract on PubMed

Topics

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

Share to DNA Breaks, Double-Stranded
Share to Dose-Response Relationship, Radiation

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Endodeoxyribonucleases

Share to Endonucleases

Share to Rad51 Recombinase

Share to Rad52 DNA Repair and Recombination Protein

Share to Replication Protein C

Share to Transcription Factor TFIIH

Source

Identifiers

PMID: 20227372
DOI: 10.1016/j.molcel.2010.02.008

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A postincision-deficient TFIIH causes replication fork breakage and uncovers alternative Rad51- or Pol32-mediated restart mechanisms.PMID 20227372Read ↗

Replication fork breakage and re-start: New insights into Rad3/XPD-associated deficiencies.Semantic proximity Read ↗

The rem mutations in the ATP-binding groove of the Rad3/XPD helicase lead to Xeroderma pigmentosum-Cockayne syndrome-like phenotypes.Semantic proximity Read ↗

DNA2 drives processing and restart of reversed replication forks in human cellsSemantic proximity Read ↗

Generation of DNA single-strand displacement by compromised nucleotide excision repair.Semantic proximity Read ↗

Disease-associated DNA2 nuclease-helicase protects cells from lethal chromosome under-replication.Semantic proximity Read ↗

Non-enzymatic roles of human RAD51 at stalled replication forksSemantic proximity Read ↗

The histone variant H2A.Z is required for efficient transcription-coupled NER and to maintain genome integrity in UV challenged yeast cellsSemantic proximity Read ↗

Error-free DNA damage tolerance and sister chromatid proximity during DNA replication rely on the Polα/Primase/Ctf4 Complex.Semantic proximity Read ↗

High-Resolution Mapping of Homologous Recombination Events in rad3 Hyper-Recombination Mutants in Yeast.Semantic proximity Read ↗

Ultrafine anaphase bridges, broken DNA and illegitimate recombination induced by a replication fork barrier.Semantic proximity Read ↗

Rad51 determines pathway usage in post-replication repair.Semantic proximity Read ↗

Hyper-Acetylation of Histone H3K56 Limits Break-Induced Replication by Inhibiting Extensive Repair Synthesis.Semantic proximity Read ↗

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