ArticleNucleic acids research2016
A phospho-dependent mechanism involving NCoR and KMT2D controls a permissive chromatin state at Notch target genes.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 100 citations in OpenAlex.
- Investigating the Antiviral Mechanism of Kaempferol Against Grouper Iridovirus: Combined Evaluation of In Vitro Activity and In Vivo Efficacy.Journal of fish diseases · 2026Article
- SPEN Loss Drives Extrafollicular Diffuse Large B-cell Lymphoma with Female-Specific Lethality and Therapeutic Vulnerabilities.Cancer discovery · 2026Article
- Histone methyltransferase KMT2D promotes castration-resistant prostate cancer progression by reactivating AR through FOXA1.Oncogene · 2026Article
- Set1 promotes Notch-induced transcriptional activation.Cellular and molecular life sciences : CMLS · 2026Article
- Article
- Article
- Tobacco smoke carcinogens exacerbate APOBEC mutagenesis and carcinogenesis.Research square · 2025Article
- Article
- Tobacco smoke carcinogens exacerbate APOBEC mutagenesis and carcinogenesis.bioRxiv : the preprint server for biology · 2025Article
- Loss of Notch dimerization perturbs intestinal homeostasis by a mechanism involving HDAC activity.PLoS genetics · 2024Article
- KMT2D-mediated H3K4me1 recruits YBX1 to facilitate triple-negative breast cancer progression through epigenetic activation of c-Myc.Clinical and translational medicine · 2024Article
- Comprehensive genomic features indicative for Notch responsiveness.Nucleic acids research · 2024Article
- Article
- Molecular insights of KMT2D and clinical aspects of Kabuki syndrome type 1.Birth defects research · 2023Review
- IndiSPENsable for X Chromosome Inactivation and Gene Silencing.Epigenomes · 2023Review
- Article
- Modulation of Notch Signaling by Small-Molecular Compounds and Its Potential in Anticancer Studies.Cancers · 2023Review
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- The SPOC domain is a phosphoserine binding module that bridges transcription machinery with co- and post-transcriptional regulators.Nature communications · 2023Article
- The structure, binding and function of a Notch transcription complex involving RBPJ and the epigenetic reader protein L3MBTL3.Nucleic acids research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
The transcriptional shift from repression to activation of target genes is crucial for the fidelity of Notch responses through incompletely understood mechanisms that likely involve chromatin-based control. To activate silenced genes, repressive chromatin marks are removed and active marks must be acquired. Histone H3 lysine-4 (H3K4) demethylases are key chromatin modifiers that establish the repressive chromatin state at Notch target genes. However, the counteracting histone methyltransferase required for the active chromatin state remained elusive. Here, we show that the RBP-J interacting factor SHARP is not only able to interact with the NCoR corepressor complex, but also with the H3K4 methyltransferase KMT2D coactivator complex. KMT2D and NCoR compete for the C-terminal SPOC-domain of SHARP. We reveal that the SPOC-domain exclusively binds to phosphorylated NCoR. The balance between NCoR and KMT2D binding is shifted upon mutating the phosphorylation sites of NCoR or upon inhibition of the NCoR kinase CK2β. Furthermore, we show that the homologs of SHARP and KMT2D in Drosophila also physically interact and control Notch-mediated functions in vivo Together, our findings reveal how signaling can fine-tune a committed chromatin state by phosphorylation of a pivotal chromatin-modifier.
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.