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

Pyrimidine Pool Disequilibrium Induced by a Cytidine Deaminase Deficiency Inhibits PARP-1 Activity, Leading to the Under Replication of DNA

16 Jul 2015

Abstract excerpt

Genome stability is jeopardized by imbalances of the dNTP pool; such imbalances affect the rate of fork progression. For example, cytidine deaminase (CDA) deficiency leads to an excess of dCTP, slowing the replication fork. We describe here a novel mechanism by which pyrimidine pool disequilibrium compromises the completion of replication and chromosome segregation: the intracellular accumulation of dCTP inhibits...

Read the complete abstract on PubMed

Topics

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

Share to DNA Repair Mechanisms
Share to PARP inhibition in cancer therapy

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 26181065
DOI: 10.1371/journal.pgen.1005384

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

Pyrimidine Pool Disequilibrium Induced by a Cytidine Deaminase Deficiency Inhibits PARP-1 Activity, Leading to the Under Replication of DNAPMID 26181065Read ↗

Bloom helicase and DNA topoisomerase IIIalpha are involved in the dissolution of sister chromatids.Semantic proximity Read ↗

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

Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome.Semantic proximity Read ↗

A novel cell-cycle-regulated interaction of the Bloom syndrome helicase BLM with Mcm6 controls replication-linked processes.Semantic proximity Read ↗

A decrease in NAMPT activity impairs basal PARP-1 activity in cytidine deaminase deficient-cells, independently of NAD.Semantic proximity Read ↗

BLM helicase suppresses recombination at G-quadruplex motifs in transcribed genesSemantic proximity Read ↗

Aberrant chromosome morphology in human cells defective for Holliday junction resolution.Semantic proximity Read ↗

Regulation and Localization of the Bloom Syndrome Protein in Response to DNA DamageSemantic proximity Read ↗

Mechanism of Bloom syndrome complex assembly required for double Holliday junction dissolution and genome stability.Semantic proximity Read ↗

Characterising replisome disassembly in human cellsSemantic proximity Read ↗

The BLM helicase contributes to telomere maintenance through processing of late-replicating intermediate structuresSemantic proximity Read ↗

Absence of BLM leads to accumulation of chromosomal DNA breaks during both unperturbed and disrupted S phasesSemantic proximity Read ↗

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