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

Locus-specific transcription silencing at the FHIT gene suppresses replication stress-induced copy number variant formation and associated replication delay.

Nucleic acids research - 21 Jul 2021

Park So Hae, Bennett-Baker Pamela, Ahmed Samreen, Arlt Martin F, Ljungman Mats, Glover Thomas W, Wilson Thomas E

Abstract excerpt

Impaired replication progression leads to de novo copy number variant (CNV) formation at common fragile sites (CFSs). We previously showed that these hotspots for genome instability reside in late-replicating domains associated with large transcribed genes and provided indirect evidence that transcription is a factor in their instability. Here, we compared aphidicolin (APH)-induced CNV and CFS frequency between...

Read the complete abstract on PubMed

Topics

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

Share to Acid Anhydride Hydrolases
Share to Aphidicolin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromosome Fragile Sites

Share to DNA Copy Number Variations

Share to DNA Replication

Share to Genetic Loci

Share to Ribonuclease H

Share to Stress, Physiological

Source

Open in PubMed Open full text

Identifiers

PMID: 34181717
DOI: 10.1093/nar/gkab559
PMCID: PMC8287918

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Locus-specific transcription silencing at the FHIT gene suppresses replication stress-induced copy number variant formation and associated replication delay.PMID 34181717Read ↗

Replication stress and mechanisms of CNV formation.Semantic proximity Read ↗

Replication stress induces genome-wide copy number changes in human cells that resemble polymorphic and pathogenic variants.Semantic proximity Read ↗

Copy number variants are produced in response to low-dose ionizing radiation in cultured cells.Semantic proximity Read ↗

Comparison of constitutional and replication stress-induced genome structural variation by SNP array and mate-pair sequencing.Semantic proximity Read ↗

Transcription-mediated organization of the replication initiation program across large genes sets up common fragile sites genome-wideSemantic proximity Read ↗

Translesion polymerase eta both facilitates DNA replication and promotes increased human genetic variation at common fragile sites.Semantic proximity Read ↗

Replication stress causes delayed mitotic entry and Chromosome 12 fragility at the ANKS1B large neuronal gene in human induced pluripotent stem cellsSemantic proximity Read ↗

Hydroxyurea induces de novo copy number variants in human cells.Semantic proximity Read ↗

Transcription-dependent regulation of replication dynamics modulates genome stabilitySemantic proximity Read ↗

Genome-wide mapping and profiling of γH2AX binding hotspots in response to different replication stress inducersSemantic proximity Read ↗

Mechanisms of genomic instabilities underlying two common fragile-site-associated loci, PARK2 and DMD, in germ cell and cancer cell lines.Semantic proximity Read ↗

Time- and cell-dependent atypia and cell death are caused by progressive deficiency in DNA replicationSemantic proximity Read ↗

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