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

Phosphorylation of a C-terminal auto-inhibitory domain increases SMARCAL1 activity.

Nucleic acids research - 1 Jan 2014

Carroll Clinton, Bansbach Carol E, Zhao Runxiang, Jung Sung Yun, Qin Jun, Cortez David

Abstract excerpt

SMARCAL1 promotes the repair and restart of damaged replication forks. Either overexpression or silencing SMARCAL1 causes the accumulation of replication-associated DNA damage. SMARCAL1 is heavily phosphorylated. Here we identify multiple phosphorylation sites, including S889, which is phosphorylated even in undamaged cells. S889 is highly conserved through evolution and it regulates SMARCAL1 activity....

Read the complete abstract on PubMed

Topics

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

Share to Amino Acid Sequence
Share to Cell Line
Share to DNA Helicases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to HEK293 Cells

Share to Molecular Sequence Data

Share to Mutation

Share to Phosphorylation

Share to Protein Structure, Tertiary

Source

Open in PubMed Open full text

Identifiers

PMID: 24150942
DOI: 10.1093/nar/gkt929
PMCID: PMC3902923

Genes

SMARCAL1

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

Phosphorylation of a C-terminal auto-inhibitory domain increases SMARCAL1 activity.PMID 24150942Read ↗

SMARCAD1 Regulates R-Loops at Active Replication Forks Linked to Cancer Mutation HotspotsSemantic proximity Read ↗

The annealing helicase SMARCAL1 maintains genome integrity at stalled replication forks.Semantic proximity Read ↗

SMARCA4 deficiency-associated heterochromatin induces intrinsic DNA replication stress and susceptibility to ATR inhibition in lung adenocarcinomaSemantic proximity Read ↗

Identification of SMARCAL1 as a component of the DNA damage response.Semantic proximity Read ↗

A consensus set of genetic vulnerabilities to ATR inhibitionSemantic proximity Read ↗

Functions of SMARCAL1, ZRANB3, and HLTF in maintaining genome stability.Semantic proximity Read ↗

Defective replication stress response inhibits lymphomagenesis and impairs lymphocyte reconstitution.Semantic proximity Read ↗

DNA Damage-Induced, S-Phase Specific Phosphorylation of Orc6 is Critical for the Maintenance of Genome StabilitySemantic proximity Read ↗

The phosphoproteomic landscape of the DNA damage responseSemantic proximity Read ↗

In-Depth Mapping of DNA-PKcs Signaling Uncovers Conserved Features of Its Kinase SpecificitySemantic proximity Read ↗

Histone Phosphorylation in DNA Damage ResponseSemantic 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.