ArticleStructure (London, England : 1993)2015
The SWI/SNF Subunit INI1 Contains an N-Terminal Winged Helix DNA Binding Domain that Is a Target for Mutations in Schwannomatosis.
Article in Structure (London, England : 1993), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- SMARCB1 missense mutants disrupt SWI/SNF complex stability and remodeling activity.Nature communications · 2026Article
- Molecular pathogenesis of the schwannomatosis genes and genetic testing strategies.Familial cancer · 2025Review
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- TAR RNA Mimicry of INI1 and Its Influence on Non-Integration Function of HIV-1 Integrase.Viruses · 2025Review
- Structure of the nucleosome-bound human BCL7A.Nucleic acids research · 2025Article
- A novel mutation in SMARCB1 associated with adult Coffin-Siris syndrome and meningioma.Acta biochimica et biophysica Sinica · 2024Article
- Chromatin remodellers as therapeutic targets.Nature reviews. Drug discovery · 2024Review
- Review
- Modeling human brain rhabdoid tumor by inactivating tumor suppressor genes in induced pluripotent stem cells.Bioactive materials · 2024Article
- A Carboxy-terminal Smarcb1 Point Mutation Induces Hydrocephalus Formation and Affects AP-1 and Neuronal Signalling Pathways in Mice.Cellular and molecular neurobiology · 2023Article
- Recent insights into the SWI/SNF complex and the molecular mechanism of hSNF5 deficiency in rhabdoid tumors.Cancer medicine · 2023Review
- Structure of nucleosome-bound human PBAF complex.Nature communications · 2022Article
- Review
- Schwannomatosis patient who was followed up for fifteen years: A case report.World journal of clinical cases · 2022Article
- Article
- Immunotherapy for SMARCB1-Deficient Sarcomas: Current Evidence and Future Developments.Biomedicines · 2022Review
- Inhibition of nuclear export restores nuclear localization and residual tumor suppressor function of truncated SMARCB1/INI1 protein in a molecular subset of atypical teratoid/rhabdoid tumors.Acta neuropathologica · 2021Article
- Chromatin remodelling complexes in cerebral cortex development and neurodevelopmental disorders.Neurochemistry international · 2021Article
- SWI/SNF subunit BAF155 N-terminus structure informs the impact of cancer-associated mutations and reveals a potential drug binding site.Communications biology · 2021Article
- Exploiting vulnerabilities of SWI/SNF chromatin remodelling complexes for cancer therapy.Oncogene · 2021Review
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 2 institutions in 2 countries.
Funding
Abstract
SWI/SNF complexes use the energy of ATP hydrolysis to remodel chromatin. In mammals they play a central role in regulating gene expression during differentiation and proliferation. Mutations in SWI/SNF subunits are among the most frequent gene alterations in cancer. The INI1/hSNF5/SMARCB1 subunit is mutated in both malignant rhabdoid tumor, a highly aggressive childhood cancer, and schwannomatosis, a tumor-predisposing syndrome characterized by mostly benign tumors of the CNS. Here, we show that mutations in INI1 that cause schwannomatosis target a hitherto unidentified N-terminal winged helix DNA binding domain that is also present in the BAF45a/PHF10 subunit of the SWI/SNF complex. The domain is structurally related to the SKI/SNO/DAC domain, which is found in a number of metazoan chromatin-associated proteins.
Indexed as
Identifiers
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.