ArticleNature communications2019
Satb1 integrates DNA binding site geometry and torsional stress to differentially target nucleosome-dense regions.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed.
- Aging-associated SATB1 deficiency remodels 3D genome architecture and transcriptional programs in naive CD4Science advances · 2026Article
- SATB1 preserves CD4Life science alliance · 2026Article
- SATB1 in cancer progression and metastasis: mechanisms and therapeutic potential.Frontiers in oncology · 2025Review
- Structural Basis of Nucleic Acid Recognition and 6mA Demethylation byInternational journal of molecular sciences · 2024Article
- SATB1 Chromatin Loops Regulate Megakaryocyte/Erythroid Progenitor Expansion by Facilitating HSP70 and GATA1 Induction.Stem cells (Dayton, Ohio) · 2023Article
- A novel SATB1 protein isoform with different biophysical properties.Frontiers in cell and developmental biology · 2023Article
- Mechanical determinants of chromatin topology and gene expression.Nucleus (Austin, Tex.) · 2022Review
- The 3D enhancer network of the developing T cell genome is shaped by SATB1.Nature communications · 2022Article
- SATB1 ensures appropriate transcriptional programs within naïve CD8Immunology and cell biology · 2022Article
- Enhancer-Mediated Formation of Nuclear Transcription Initiation Domains.International journal of molecular sciences · 2022Review
- Downregulation of SATB1 by miRNAs reduces megakaryocyte/erythroid progenitor expansion in preclinical models of Diamond-Blackfan anemia.Experimental hematology · 2022Article
- MicroRNA-409 regulates the proliferation and invasion of breast cancer cell lines by targeting special AT-rich sequence-binding protein 1 (SATB1).Bioengineered · 2022Article
- 3D Genome Organization as an Epigenetic Determinant of Transcription Regulation in T Cells.Frontiers in immunology · 2022Review
- SATB1, genomic instability and Gleason grading constitute a novel risk score for prostate cancer.Scientific reports · 2021Article
- ZFP451-mediated SUMOylation of SATB2 drives embryonic stem cell differentiation.Genes & development · 2021Article
- Base-resolution models of transcription-factor binding reveal soft motif syntax.Nature genetics · 2021Article
- Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction.American journal of human genetics · 2021Article
- The Causes and Consequences of Spatial Organization of the Genome in Regulation of Gene Expression.Frontiers in immunology · 2021Review
- Article
- SATB1-mediated chromatin landscape in T cells.Nucleus (Austin, Tex.) · 2020Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The Satb1 genome organizer regulates multiple cellular and developmental processes. It is not yet clear how Satb1 selects different sets of targets throughout the genome. Here we have used live-cell single molecule imaging and deep sequencing to assess determinants of Satb1 binding-site selectivity. We have found that Satb1 preferentially targets nucleosome-dense regions and can directly bind consensus motifs within nucleosomes. Some genomic regions harbor multiple, regularly spaced Satb1 binding motifs (typical separation ~1 turn of the DNA helix) characterized by highly cooperative binding. The Satb1 homeodomain is dispensable for high affinity binding but is essential for specificity. Finally, we find that Satb1-DNA interactions are mechanosensitive. Increasing negative torsional stress in DNA enhances Satb1 binding and Satb1 stabilizes base unpairing regions against melting by molecular machines. The ability of Satb1 to control diverse biological programs may reflect its ability to combinatorially use multiple site selection criteria.
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