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

The Rad53CHK1/CHK2-Spt21NPAT and Tel1ATM axes couple glucose tolerance to histone dosage and subtelomeric silencing.

Nature communications - 19 Aug 2020

Bruhn Christopher, Ajazi Arta, Ferrari Elisa, Lanz Michael Charles, Batrin Renaud, Choudhary Ramveer, Walvekar Adhish, Laxman Sunil, Longhese Maria Pia, Fabre Emmanuelle, Smolka Marcus Bustamente, Foiani Marco

Abstract excerpt

The DNA damage response (DDR) coordinates DNA metabolism with nuclear and non-nuclear processes. The DDR kinase Rad53CHK1/CHK2 controls histone degradation to assist DNA repair. However, Rad53 deficiency causes histone-dependent growth defects in the absence of DNA damage, pointing out unknown physiological functions of the Rad53-histone axis. Here we show that histone dosage control by Rad53 ensures metabolic...

Read the complete abstract on PubMed

Topics

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

Share to Acetylation
Share to Ataxia Telangiectasia Mutated Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Checkpoint Kinase 2

Share to Gene Silencing

Share to Glucose

Share to Histone Deacetylases

Share to Serine

Share to Telomere

Source

Open in PubMed Open full text

Identifiers

PMID: 32814778
DOI: 10.1038/s41467-020-17961-4
PMCID: PMC7438486

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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

The Rad53CHK1/CHK2-Spt21NPAT and Tel1ATM axes couple glucose tolerance to histone dosage and subtelomeric silencing.PMID 32814778Read ↗

Yeast Nuak1 phosphorylates histone H3 threonine 11 in low glucose stress conditions by the cooperation of AMPK and CK2 signalingSemantic proximity Read ↗

H2A Monoubiquitination Links Glucose Availability to Epigenetic Regulation of the Endoplasmic Reticulum Stress Response and Cancer Cell DeathSemantic proximity Read ↗

A Rad53 kinase-dependent surveillance mechanism that regulates histone protein levels in S. cerevisiae.Semantic proximity Read ↗

Saccharomyces cerevisiae TORC1 Controls Histone Acetylation by Signaling Through the Sit4/PP6 Phosphatase to Regulate Sirtuin Deacetylase Nuclear Accumulation.Semantic proximity Read ↗

Metabolic regulation by p53 prevents R-loop-associated genomic instabilitySemantic proximity Read ↗

Metabolic regulation of telomere silencing by SESAME complex-catalyzed H3T11 phosphorylationSemantic proximity Read ↗

The INO80 Chromatin Remodeler Sustains Metabolic Stability by Promoting TOR Signaling and Regulating Histone AcetylationSemantic proximity Read ↗

Histone H3 K56 hyperacetylation perturbs replisomes and causes DNA damage.Semantic proximity Read ↗

Genomewide screen for negative regulators of sirtuin activity in Saccharomyces cerevisiae reveals 40 loci and links to metabolism.Semantic proximity Read ↗

Genetic interaction of RAD53 protein kinase with histones is important for DNA replication.Semantic proximity Read ↗

Pancreatic cancers suppress negative feedback of glucose transport to reprogram chromatin for metastasisSemantic proximity Read ↗

Feedback Control of p53 Translation by REDD1 and mTORC1 Limits the p53-Dependent DNA Damage ResponseSemantic proximity Read ↗

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