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

Cullin3-KLHL15 ubiquitin ligase mediates CtIP protein turnover to fine-tune DNA-end resection.

Nature communications - 26 Aug 2016

Ferretti Lorenza P, Himmels Sarah-Felicitas, Trenner Anika, Walker Christina, von Aesch Christine, Eggenschwiler Aline, Murina Olga, Enchev Radoslav I, Peter Matthias, Freire Raimundo, Porro Antonio, Sartori Alessandro A

Abstract excerpt

Human CtIP is a decisive factor in DNA double-strand break repair pathway choice by enabling DNA-end resection, the first step that differentiates homologous recombination (HR) from non-homologous end-joining (NHEJ). To coordinate appropriate and timely execution of DNA-end resection, CtIP function is tightly controlled by multiple protein-protein interactions and post-translational modifications. Here, we...

Read the complete abstract on PubMed

Topics

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

Share to Cullin Proteins
Share to DNA Breaks, Double-Stranded

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA End-Joining Repair

Share to Endodeoxyribonucleases

Share to Homologous Recombination

Share to Protein Interaction Domains and Motifs

Share to Proteolysis

Share to Ubiquitination

Source

Open in PubMed Open full text

Identifiers

PMID: 27561354
DOI: 10.1038/ncomms12628
PMCID: PMC5007465

Genes

KLHL15
FRY

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.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cullin3-KLHL15 ubiquitin ligase mediates CtIP protein turnover to fine-tune DNA-end resection.PMID 27561354Read ↗

Human HELQ regulates DNA end resection at DNA double-strand breaks and stalled replication forksSemantic proximity Read ↗

RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand BreaksSemantic proximity Read ↗

SIAH2 regulates DNA end resection and replication fork recovery by promoting CtIP ubiquitinationSemantic proximity Read ↗

The yeast Fun30 and human SMARCAD1 chromatin remodellers promote DNA end resection.Semantic proximity Read ↗

The E3 ubiquitin ligase DTX3L and the deubiquitinase USP28 fine-tune DNA double strand repair through mutual regulation of their protein levelsSemantic proximity Read ↗

DNA double-strand break end resection: a critical relay point for determining the pathway of repair and signalingSemantic proximity Read ↗

DNA End Resection: Facts and MechanismsSemantic proximity Read ↗

Single-Strand Break End Resection in Genome Integrity: Mechanism and Regulation by APE2Semantic proximity Read ↗

The pendulum of the Ku-Ku clockSemantic proximity Read ↗

The human HELLS chromatin remodelling protein promotes end resection to facilitate homologous recombination and contributes to DSB repair within heterochromatinSemantic proximity Read ↗

Controlling DNA-end resection: a new task for CDKsSemantic proximity Read ↗

EXO5-DNA structure and BLM interactions direct DNA resection critical for ATR-dependent replication restart.Semantic proximity Read ↗

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