ArticleNucleic acids research2014
Phosphorylation of a C-terminal auto-inhibitory domain increases SMARCAL1 activity.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Mechanisms and regulation of replication fork reversal.DNA repair · 2024Review
- SMARCAL1 ubiquitylation controls its association with RPA-coated ssDNA and promotes replication fork stability.PLoS biology · 2024Article
- Adenovirus E1B 55-Kilodalton Protein Targets SMARCAL1 for Degradation during Infection and Modulates Cellular DNA Replication.Journal of virology · 2019Article
- Whole Exome Sequencing Identified a Novel BiallelicFrontiers in genetics · 2019Article
- Article
- Mechanisms for stalled replication fork stabilization: new targets for synthetic lethality strategies in cancer treatments.EMBO reports · 2018Review
- Functions of SMARCAL1, ZRANB3, and HLTF in maintaining genome stability.Critical reviews in biochemistry and molecular biology · 2017Review
- Replication fork reversal in eukaryotes: from dead end to dynamic response.Nature reviews. Molecular cell biology · 2015Review
- Structural analysis of replication protein A recruitment of the DNA damage response protein SMARCAL1.Biochemistry · 2014Article
- HARP preferentially co-purifies with RPA bound to DNA-PK and blocks RPA phosphorylation.Epigenetics · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
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. Specifically, S889 phosphorylation increases the DNA-stimulated ATPase activity of SMARCAL1 and increases its ability to catalyze replication fork regression. A phosphomimetic S889 mutant is also hyperactive when expressed in cells, while a non-phosphorylatable mutant is less active. S889 lies within a C-terminal region of the SMARCAL1 protein. Deletion of the C-terminal region also creates a hyperactive SMARCAL1 protein suggesting that S889 phosphorylation relieves an auto-inhibitory function of this SMARCAL1 domain. Thus, S889 phosphorylation is one mechanism by which SMARCAL1 activity is regulated to ensure the proper level of fork remodeling needed to maintain genome integrity during DNA synthesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.