Systematic analysis of linker histone PTM hotspots reveals phosphorylation sites that modulate homologous recombination and DSB repair.

doi:10.1016/j.dnarep.2019.102763

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

Community

Back to search

Article

Systematic analysis of linker histone PTM hotspots reveals phosphorylation sites that modulate homologous recombination and DSB repair.

DNA repair - 1 Feb 2020

Mukherjee Kuntal, English Nolan, Meers Chance, Kim Hyojung, Jonke Alex, Storici Francesca, Torres Matthew

Abstract excerpt

Double strand-breaks (DSBs) of genomic DNA caused by ionizing radiation or mutagenic chemicals are a common source of mutation, recombination, chromosomal aberration, and cell death. Linker histones are DNA packaging proteins with established roles in chromatin compaction, gene transcription, and in homologous recombination (HR)-mediated DNA repair. Using a machine-learning model for functional prioritization of...

Read the complete abstract on PubMed

Topics

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

Share to DNA Breaks, Double-Stranded
Share to DNA, Fungal

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

Share to Histones

Share to Homologous Recombination

Share to Machine Learning

Share to Phosphorylation

Share to Protein Processing, Post-Translational

Share to Saccharomyces cerevisiae Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 31821952
DOI: 10.1016/j.dnarep.2019.102763
PMCID: PMC6996138

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.