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

Functional Mutations Form at CTCF-Cohesin Binding Sites in Melanoma Due to Uneven Nucleotide Excision Repair across the Motif.

Cell reports - 13 Dec 2016

Poulos Rebecca C, Thoms Julie A I, Guan Yi Fang, Unnikrishnan Ashwin, Pimanda John E, Wong Jason W H

Abstract excerpt

CTCF binding sites are frequently mutated in cancer, but how these mutations accumulate and whether they broadly perturb CTCF binding are not well understood. Here, we report that skin cancers exhibit a highly specific asymmetric mutation pattern within CTCF motifs attributable to ultraviolet irradiation and differential nucleotide excision repair (NER). CTCF binding site mutations form independently of...

Read the complete abstract on PubMed

Topics

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

Share to CCCTC-Binding Factor
Share to Cell Cycle Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromatin

Share to Chromosomal Proteins, Non-Histone

Share to Cohesins

Share to DNA Repair

Share to Melanoma

Share to Transcription, Genetic

Source

Identifiers

PMID: 27974201
DOI: 10.1016/j.celrep.2016.11.055

Genes

CTCF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Functional Mutations Form at CTCF-Cohesin Binding Sites in Melanoma Due to Uneven Nucleotide Excision Repair across the Motif.PMID 27974201Read ↗

Nucleotide excision repair is impaired by binding of transcription factors to DNASemantic proximity Read ↗

CTCF binding modulates UV damage formation to promote mutation hot spots in melanoma.Semantic proximity Read ↗

ETS transcription factors induce a unique UV damage signature that drives recurrent mutagenesis in melanoma.Semantic proximity Read ↗

Multiple interaction nodes define the postreplication repair response to UV-induced DNA damage that is defective in melanomas and correlated with UV signature mutation load.Semantic proximity Read ↗

Therapy-associated mutagenesis at CTCF binding sites is shaped by chromatin context and DNA repair capacitySemantic proximity Read ↗

CTCF Binding Site Mutations: Linking Topologically Associated Domains Dysregulation to Cutaneous Squamous Cell Carcinoma ProgressionSemantic proximity Read ↗

Melanoma-specific mutation hotspots in distal, non-coding, promoter-interacting regions implicate novel candidate driver genes.Semantic proximity Read ↗

Decoding Cancer Variants of Unknown Significance for Helicase–Nuclease–RPA Complexes Orchestrating DNA Repair During Transcription and ReplicationSemantic proximity Read ↗

Detecting recurrent passenger mutations in melanoma by targeted UV damage sequencing.Semantic proximity Read ↗

Clustered somatic mutations are frequent in transcription factor binding motifs within proximal promoter regions in melanoma and other cutaneous malignancies.Semantic proximity Read ↗

Disruption of CTCF binding by germline non-coding variants in <i>CDKN2B</i> suppress <i>CDKN2A</i> expression and predispose to melanomaSemantic proximity Read ↗

ERCC2 mutations alter the genomic distribution pattern of somatic mutations and are independently prognostic in bladder cancer.Semantic proximity Read ↗

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