ArticleEMBO reports2008
Atrophin recruits HDAC1/2 and G9a to modify histone H3K9 and to determine cell fates.
Article in EMBO reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 85 citations in OpenAlex.
- NRSF regulation of OPRM1 through histone acetylation.Clinical epigenetics · 2026Article
- A de novo missense variant in MIDEAS results in increased deacetylase activity of the MiDAC HDAC complex causing a neurodevelopmental syndrome.Nature communications · 2025Article
- A de novo variant of RERE was identified in a patient with neurodevelopmental disorder, enuresis and scoliosis.Scientific reports · 2025Article
- CircRNAs expression profile and potential roles of circRERE-PMN in pre-metastatic lungs.Frontiers in immunology · 2024Article
- Functional implications of paralog genes in polyglutamine spinocerebellar ataxias.Human genetics · 2023Review
- A potential histone-chaperone activity for the MIER1 histone deacetylase complex.Nucleic acids research · 2023Article
- Zebrafish model of RERE syndrome recapitulates key ophthalmic defects that are rescued by small molecule inhibitor of shh signaling.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Whole-genome functional characterization of RE1 silencers using a modified massively parallel reporter assay.Cell genomics · 2023Article
- Distinct biochemical properties of the class I histone deacetylase complexes.Current opinion in chemical biology · 2022Review
- High-Content Drug Discovery Targeting Molecular Bladder Cancer Subtypes.International journal of molecular sciences · 2022Article
- Hypoxia-Inducible Lysine Methyltransferases: G9a and GLP Hypoxic Regulation, Non-histone Substrate Modification, and Pathological Relevance.Frontiers in genetics · 2020Review
- Germinal center-derived lymphomas: The darkest side of humoral immunity.Immunological reviews · 2019Review
- Targeting the GFI1/1B-CoREST Complex in Acute Myeloid Leukemia.Frontiers in oncology · 2019Review
- RERE deficiency leads to decreased expression of GATA4 and the development of ventricular septal defects.Disease models & mechanisms · 2018Article
- Genotype-phenotype correlations in individuals with pathogenic RERE variants.Human mutation · 2018Article
- The histone deacetylase HDAC1 positively regulates Notch signaling duringBiology open · 2018Article
- Machine Learning Analysis IdentifiesG3 (Bethesda, Md.) · 2017Article
- The WHHERE coactivator complex is required for retinoic acid-dependent regulation of embryonic symmetry.Nature communications · 2017Article
- Atrophin controls developmental signaling pathways via interactions with Trithorax-like.eLife · 2017Article
- The expanding role of the Ehmt2/G9a complex in neurodevelopment.Neurogenesis (Austin, Tex.) · 2017Article
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 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrophin family proteins, including the vertebrate arginine-glutamic acid dipeptide repeats protein (RERE) and Drosophila Atrophin (Atro), constitute a new class of nuclear receptor corepressors. Both RERE and Atro share the ELM2 (EGL-27 and MTA1 homology 2) and SANT (SWI3/ADA2/N-CoR/TFIII-B) domains, which are also present in other important transcriptional cofactors. Here, we report that the SANT domain in RERE binds to the histone methyltransferase G9a, and that both the ELM2 and SANT domains orchestrate molecular events that lead to a stable methylation of histone H3-lysine 9. We establish the physiological relevance of these interactions among Atrophin, G9a, and histone deacetylases 1 and 2 in Drosophila by showing that these proteins localize to overlapping chromosomal loci, and act together to suppress wing vein and melanotic-mass formation. This study not only shows a new function of the SANT domain and establishes its connection with the ELM2 domain, but also implies that a similar strategy is used by other ELM2-SANT proteins to repress gene transcription and to exert biological effects.
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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.