ReviewEpigenetics2014
Crosstalk between epigenetic readers regulates the MOZ/MORF HAT complexes.
Review in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed.
- Histone modification cross-talk: analytical tools and molecular mechanisms.The Biochemical journal · 2026Review
- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- BRPF1 in cancer epigenetics: a key regulator of histone acetylation and a promising therapeutic target.Cell death discovery · 2025Review
- Chromatin-focused genetic and chemical screens identify BRPF1 as a targetable vulnerability in Taxol-resistant triple-negative breast cancer.Experimental & molecular medicine · 2025Article
- Molecular and clinical aspects of histone-related disorders.Human genomics · 2025Review
- A multivalent engagement of ENL with MOZ.Nature structural & molecular biology · 2025Article
- Epigene functional diversity: isoform usage, disordered domain content, and variable binding partners.Epigenetics & chromatin · 2025Article
- Bromodomain and PHD Finger-Containing Protein 1: From Functions to a Developmental Disorder, Cancer, and Therapeutics.Results and problems in cell differentiation · 2025Review
- The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency.Journal of hematology & oncology · 2024Article
- HBO1, a MYSTerious KAT and its links to cancer.Biochimica et biophysica acta. Gene regulatory mechanisms · 2024Review
- A MOZ-TIF2 leukemia mouse model displays KAT6-dependent H3K23 propionylation and overexpression of a set of active developmental genes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- A massive alteration of gene expression in undescended testicles of dogs and the association ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- DOT1L interaction partner AF10 controls patterning of H3K79 methylation and RNA polymerase II to maintain cell identity.Stem cell reports · 2023Article
- Clinical features and underlying mechanisms of KAT6B disease in a Chinese boy.Molecular genetics & genomic medicine · 2023Article
- Tctp, a unique Ing5-binding partner, inhibits the chromatin binding of Enok inProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Targeting Proliferation Signals and the Cell Cycle Machinery in Acute Leukemias: Novel Molecules on the Horizon.Molecules (Basel, Switzerland) · 2023Review
- The histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA binding winged helix domain.Nucleic acids research · 2023Article
- Role of the MOZ/MLL-mediated transcriptional activation system for self-renewal in normal hematopoiesis and leukemogenesis.The FEBS journal · 2022Review
- Hydrophobic cavity-directed azide-acetyllysine photochemistry for profiling non-histone interacting partners of bromodomain protein 1.RSC chemical biology · 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
5 authors.
Funding
Abstract
The MOZ/MORF complexes represent an example of a chromatin-binding assembly whose recruitment to specific genomic regions and activity can be fine-tuned by posttranslational modifications of histones. Here we detail the structures and biological functions of epigenetic readers present in the four core subunits of the MOZ/MORF complexes, highlight the imperative role of combinatorial readout by the multiple readers, and discuss new research directions to advance our understanding of histone acetylation.
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.