ReviewExperimental hematology2023
The YEATS domain epigenetic reader proteins ENL and AF9 and their therapeutic value in leukemia.
Review in Experimental hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Discovery of a Highly Potent and Selective ENL Degrader.Journal of medicinal chemistry · 2026Article
- A Novel Approach to Prognostic Factors and Risk Stratification in Pediatric AML: Case Report and Literature Review.International journal of molecular sciences · 2025Review
- Anticancer benzimidazole derivatives as inhibitors of epigenetic targets: a review article.RSC advances · 2025Review
- A potent and selective ENL degrader suppresses oncogenic gene expression and leukemia progression.Science advances · 2024Article
- HOXA9 Regulome and Pharmacological Interventions in Leukemia.Advances in experimental medicine and biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies have uncovered similarities and differences between 2 highly homologous epigenetic reading proteins, namely, ENL (MLLT1) and AF9 (MLLT3) with therapeutic implications. The importance of these proteins has traditionally been exemplified by their involvement in chromosomal translocations with the mixed-lineage leukemia gene (MLL; aka KMT2a). MLL rearrangements occur in a subset of acute leukemias and generate potent oncogenic MLL-fusion proteins that impact epigenetic and transcriptional regulation. Leukemic patients with MLL rearrangements display intermediate-to-poor prognoses, necessitating further mechanistic research. Several protein complexes involved in regulating RNA polymerase II transcription and the epigenetic landscape are hijacked in MLL-r leukemia, which include ENL and AF9. Recent biochemical studies have defined a highly homologous YEATS domain in ENL and AF9 that binds acylated histones, which aids in the localization and retention of these proteins to transcriptional targets. In addition, detailed characterization of the homologous ANC-1 homology domain (AHD) on ENL and AF9 revealed differential association with transcriptional activating and repressing complexes. Importantly, CRISPR knockout screens have demonstrated a unique role for wild-type ENL in leukemic stem cell function, whereas AF9 appears important for normal hematopoietic stem cells. In this perspective, we examine the ENL and AF9 proteins with attention to recent work characterizing the epigenetic reading YEATS domains and AHD on both wild-type proteins and when fused to MLL. We summarized the drug development efforts and their therapeutic potential and assess ongoing research that has refined our understanding of how these proteins function, which continues to reveal new therapeutic avenues.
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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 Socratic graph.