ArticleJournal of molecular biology2008
Conserved themes in target recognition by the PAH1 and PAH2 domains of the Sin3 transcriptional corepressor.
Article in Journal of molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 59 citations in OpenAlex.
- Chromatin context-dependent deacetylation by the asymmetric Rpd3L.Nucleic acids research · 2026Article
- Stability and interaction defects in the Sin3A-PAH1 αα-hub domain associated with loss-of-function variants.The Journal of biological chemistry · 2026Article
- Differential control of both cell cycle-regulated and quantitative histone mRNA expression bybioRxiv : the preprint server for biology · 2026Article
- The Kelch13 compartment contains highly divergent vesicle trafficking proteins in malaria parasites.PLoS pathogens · 2023Article
- Article
- Functional characterization and comparative analysis of gene repression-mediating domains interacting with yeast pleiotropic corepressors Sin3, Cyc8 and Tup1.Current genetics · 2023Article
- Mechanism of assembly, activation and lysine selection by the SIN3B histone deacetylase complex.Nature communications · 2023Article
- A Novel Mechanism of Coactivator Recruitment by the Nurr1 Nuclear Receptor.Journal of molecular biology · 2022Article
- Forkhead transcription factor Fkh1: insights into functional regulatory domains crucial for recruitment of Sin3 histone deacetylase complex.Current genetics · 2021Article
- Comprehensive study of 28 individuals with SIN3A-related disorder underscoring the associated mild cognitive and distinctive facial phenotype.European journal of human genetics : EJHG · 2021Article
- Connecting the αα-hubs: same fold, disordered ligands, new functions.Cell communication and signaling : CCS · 2021Article
- The neuronal transcription factor Myt1L interacts via a conserved motif with the PAH1 domain of Sin3 to recruit the Sin3L/Rpd3L histone deacetylase complex.FEBS letters · 2020Article
- Evolutionary conservation of the intrinsic disorder-based Radical-Induced Cell Death1 hub interactome.Scientific reports · 2019Article
- Physical and functional interaction between SET1/COMPASS complex component CFP-1 and a Sin3S HDAC complex in C. elegans.Nucleic acids research · 2019Article
- Co-repressor, co-activator and general transcription factor: the many faces of the Sin3 histone deacetylase (HDAC) complex.The Biochemical journal · 2018Review
- Sin3A recruits Tet1 to the PAH1 domain via a highly conserved Sin3-Interaction Domain.Scientific reports · 2018Article
- Sin3a-Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency.Nucleic acids research · 2018Article
- A Structured Workflow for Mapping Human Sin3 Histone Deacetylase Complex Interactions Using Halo-MudPIT Affinity-Purification Mass Spectrometry.Molecular & cellular proteomics : MCP · 2018Article
- Global profiling of lysine reactivity and ligandability in the human proteome.Nature chemistry · 2017Article
- The potential of targeting Sin3B and its associated complexes for cancer therapy.Expert opinion on therapeutic targets · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The recruitment of chromatin-modifying coregulator complexes by transcription factors to specific sites of the genome constitutes an important step in many eukaryotic transcriptional regulatory pathways. The histone deacetylase-associated Sin3 corepressor complex is recruited by a large and diverse array of transcription factors through direct interactions with the N-terminal PAH domains of Sin3. Here, we describe the solution structures of the mSin3A PAH1 domain in the apo form and when bound to SAP25, a component of the corepressor complex. Unlike the apo-mSin3A PAH2 domain, the apo-PAH1 domain is conformationally pure and is largely, but not completely, folded. Portions of the interacting segments of both mSin3A PAH1 and SAP25 undergo folding upon complex formation. SAP25 binds through an amphipathic helix to a predominantly hydrophobic cleft on the surface of PAH1. Remarkably, the orientation of the helix is reversed compared to that adopted by NRSF, a transcription factor unrelated to SAP25, upon binding to the mSin3B PAH1 domain. The reversal in helical orientations is correlated with a reversal in the underlying PAH1-interaction motifs, echoing a theme previously described for the mSin3A PAH2 domain. The definition of these so-called type I and type II PAH1-interaction motifs has allowed us to predict the precise location of these motifs within previously experimentally characterized PAH1 binders. Finally, we explore the specificity determinants of protein-protein interactions involving the PAH1 and PAH2 domains. These studies reveal that even conservative replacements of PAH2 residues with equivalent PAH1 residues are sufficient to alter the affinity and specificity of these protein-protein interactions dramatically.
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.