ArticleScientific reports2016
The ATM- and ATR-related SCD domain is over-represented in proteins involved in nervous system development.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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
6 citing papers in PubMed, 16 citations in OpenAlex.
- Inhibition of ATR opposes glioblastoma invasion through disruption of cytoskeletal networks and integrin internalization via macropinocytosis.Neuro-oncology · 2024Article
- Noncanonical usage of stop codons in ciliates expands proteins with structurally flexible Q-rich motifs.eLife · 2024Article
- Germline CHEK2 and ATM Variants in Myeloid and Other Hematopoietic Malignancies.Current hematologic malignancy reports · 2022Review
- Identification of an evolutionarily conserved domain in Neurod1 favouring enteroendocrine versus goblet cell fate.PLoS genetics · 2022Article
- DNA damage causes rapid accumulation of phosphoinositides for ATR signaling.Nature communications · 2017Article
- A meeting at risk: Unrepaired DSBs go for broke.Nucleus (Austin, Tex.) · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATM and ATR are cellular kinases with a well-characterized role in the DNA-damage response. Although the complete set of ATM/ATR targets is unknown, they often contain clusters of S/TQ motifs that constitute an SCD domain. In this study, we identified putative ATM/ATR targets that have a conserved SCD domain across vertebrates. Using this approach, we have identified novel putative ATM/ATR targets in pathways known to be under direct control of these kinases. Our analysis has also unveiled significant enrichment of SCD-containing proteins in cellular pathways, such as vesicle trafficking and actin cytoskeleton, where a regulating role for ATM/ATR is either unknown or poorly understood, hinting at a much broader and overarching role for these kinases in the cell. Of particular note is the overrepresentation of conserved SCD-containing proteins involved in pathways related to neural development. This finding suggests that ATM/ATR could be directly involved in controlling this process, which may be linked to the adverse neurological effects observed in patients with mutations in ATM.
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Registered trials
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