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

Rad18 mediates specific mutational signatures and shapes the genomic landscape of carcinogen-induced tumorsin vivo

6 Jan 2021

Abstract excerpt

Abstract The E3 ubiquitin ligase Rad18 promotes a damage-tolerant and error-prone mode of DNA replication termed trans-lesion synthesis that is pathologically activated in cancer. However, the impact of vertebrate Rad18 on cancer genomes is not known. To determine how Rad18 affects mutagenesis in vivo, we have developed and implemented a novel computational pipeline to analyze genomes of carcinogen (7,...

Read the complete abstract on PubMed

Topics

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

Share to Cancer Genomics and Diagnostics
Share to Cancer-related Molecular Pathways
Share to DNA Repair Mechanisms

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

Source

Identifiers

PMID: 33447826
DOI: 10.1093/narcan/zcaa037

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Rad18 mediates specific mutational signatures and shapes the genomic landscape of carcinogen-induced tumorsin vivoPMID 33447826Read ↗

Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesis <i>in vivo</i>Semantic proximity Read ↗

Diverse roles of RAD18 and Y-family DNA polymerases in tumorigenesisSemantic proximity Read ↗

Trans-Lesion Synthesis and Mismatch Repair Pathway Crosstalk Defines Chemoresistance and Hypermutation Mechanisms in GlioblastomaSemantic proximity Read ↗

Trans-Lesion Synthesis and Mismatch Repair Pathway Crosstalk Defines Chemoresistance and Hypermutation Mechanisms in GlioblastomaSemantic proximity Read ↗

The therapeutic significance of mutational signatures from DNA repair deficiency in cancer.Semantic proximity Read ↗

DeconstructSigs: delineating mutational processes in single tumors distinguishes DNA repair deficiencies and patterns of carcinoma evolution.Semantic proximity Read ↗

Trans-lesion synthesis and mismatch repair pathway crosstalk defines chemoresistance and hypermutation mechanisms in glioblastomaSemantic proximity Read ↗

DNA Repair Footprint Uncovers Contribution of DNA Repair Mechanism to Mutational Signatures.Semantic proximity Read ↗

iMUT-seq: high-resolution DSB-induced mutation profiling reveals prevalent homologous-recombination dependent mutagenesis.Semantic proximity Read ↗

UV signature mutations.Semantic proximity Read ↗

Genetic modifiers of APOBEC-induced mutagenesisSemantic proximity Read ↗

The landscape of genetic alterations of UVB-induced skin tumors in DNA repair-deficient mice.Semantic proximity Read ↗

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