ArticleThe Journal of biological chemistry2009
Identification of SMARCAL1 as a component of the DNA damage response.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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
87 citing papers in PubMed, 111 citations in OpenAlex.
- SMARCAL1 is a candidate therapeutic target for ALT-positive tumors.Genes & development · 2026Article
- Mapping the genetic landscape of the DNA damage response with Cas12a-based combinatorial knockout screens.bioRxiv : the preprint server for biology · 2026Article
- The recurrence or metastasis related gene predicts the prognosis of extremity and trunk soft tissue sarcoma.Precision clinical medicine · 2025Article
- Pathogenic variants in MAEA disrupt DNA replication fork stability and are associated with developmental abnormalities in humans.Science advances · 2025Article
- Article
- HeterozygousGenes & development · 2024Article
- Mechanisms and regulation of replication fork reversal.DNA repair · 2024Review
- Profound T Lymphocyte and DNA Repair Defect Characterizes Schimke Immuno-Osseous Dysplasia.Journal of clinical immunology · 2024Article
- SMARCAL1 ubiquitylation controls its association with RPA-coated ssDNA and promotes replication fork stability.PLoS biology · 2024Article
- Article
- Review
- T-cell receptor signaling in Schimke immuno-osseous dysplasia is SMARCAL1-independent.Frontiers in immunology · 2022Article
- On the Interaction Between SMARCAL1 and BRG1.Frontiers in cell and developmental biology · 2022Article
- Time for remodeling: SNF2-family DNA translocases in replication fork metabolism and human disease.DNA repair · 2020Review
- Two replication fork remodeling pathways generate nuclease substrates for distinct fork protection factors.Science advances · 2020Article
- Review
- MCM8IP activates the MCM8-9 helicase to promote DNA synthesis and homologous recombination upon DNA damage.Nature communications · 2020Article
- A Drosophila cell-free system that senses DNA breaks and triggers phosphorylation signalling.Nucleic acids research · 2019Article
- Adenovirus E1B 55-Kilodalton Protein Targets SMARCAL1 for Degradation during Infection and Modulates Cellular DNA Replication.Journal of virology · 2019Article
- Advances in understanding DNA processing and protection at stalled replication forks.The Journal of cell biology · 2019Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
SMARCAL1 (also known as HARP) is a SWI/SNF family protein with an ATPase activity stimulated by DNA containing both single-stranded and double-stranded regions. Mutations in SMARCAL1 are associated with the disease Schimke immuno-osseous dysplasia, a multisystem autosomal recessive disorder characterized by T cell immunodeficiency, growth inhibition, and renal dysfunction. The cellular function of SMARCAL1, however, is unknown. Here, using Xenopus egg extracts and mass spectrometry, we identify SMARCAL1 as a protein recruited to double-stranded DNA breaks. SMARCAL1 binds to double-stranded breaks and stalled replication forks in both egg extract and human cells, specifically colocalizing with the single-stranded DNA binding factor RPA. In addition, SMARCAL1 interacts physically with RPA independently of DNA. SMARCAL1 is phosphorylated in a caffeine-sensitive manner in response to double-stranded breaks and stalled replication forks. It has been suggested that stalled forks can be stabilized by a mechanism involving caffeine-sensitive kinases, or they collapse and subsequently recruit Rad51 to promote homologous recombination repair. We show that depletion of SMARCAL1 from U2OS cells leads to increased frequency of RAD51 foci upon generation of stalled replication forks, indicating that fork breakdown is more prevalent in the absence of SMARCAL1. We propose that SMARCAL1 is a novel DNA damage-binding protein involved in replication fork stabilization.
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What OpenQuestion holds
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.