Evidence map›Paper›PMID 30066088›Full record

ReviewCellular and molecular life sciences : CMLS2018

ENL: structure, function, and roles in hematopoiesis and acute myeloid leukemia.

Jianbiao Zhou, Yvonne Ng, Wee-Joo Chng

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Discovery of a Highly Potent and Selective ENL Degrader.Journal of medicinal chemistry · 2026
    Article
  3. Article
  4. lncRNAlyzr: Enrichment Analysis for lncRNA Sets.Journal of molecular biology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Engineering an inducible leukemia-associated fusion protein enables large-scale ex vivo production of functional human phagocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Jianbiao ZhouCancer Science Institute of Singapore, Centre for Translational Medicine, National University of Singapore, 14 Medical Drive, Singapore, 117599, Republic of Singapore. csizjb@nus.edu.sg.ORCID http://orcid.org/0000-0002-5679-671X
Yvonne NgCancer Science Institute of Singapore, Centre for Translational Medicine, National University of Singapore, 14 Medical Drive, Singapore, 117599, Republic of Singapore.
Wee-Joo ChngCancer Science Institute of Singapore, Centre for Translational Medicine, National University of Singapore, 14 Medical Drive, Singapore, 117599, Republic of Singapore. mdccwj@nus.edu.sg.
National University of Singapore · SG

Funding

NMRC Clinician-Scientist IRG Grant CNIG11nov38the Singapore Ministry of Education's Tier 3 grants MOE2014-T3-1-006
6 · The paper itself

Abstract

ENL/MLLT1 is a distinctive member of the KMT2 family based on its structural homology. ENL is a histone acetylation reader and a critical component of the super elongation complex. ENL plays pivotal roles in the regulation of chromatin remodelling and gene expression of many important proto-oncogenes, such as Myc, Hox genes, via histone acetylation. Novel insights of the key role of the YEATS domain of ENL in the transcriptional control of leukemogenic gene expression has emerged from whole genome Crisp-cas9 studies in acute myeloid leukemia (AML). In this review, we have summarized what is currently known about the structure and function of the ENL molecule. We described the ENL's role in normal hematopoiesis, and leukemogenesis. We have also outlined the detailed molecular mechanisms underlying the regulation of target gene expression by ENL, as well as its major interacting partners and complexes involved. Finally, we discuss the emerging knowledge of different approaches for the validation of ENL as a therapeutic target and the development of small-molecule inhibitors disrupting the YEATS reader pocket of ENL protein, which holds great promise for the treatment of AML. This review will not only provide a fundamental understanding of the structure and function of ENL and update on the roles of ENL in AML, but also the development of new therapeutic strategies.

Indexed as

AcetylationChromatin Assembly and DisassemblyGene Expression Regulation, NeoplasticGenome, HumanHematopoiesisHumansLeukemia, Myeloid, AcuteNeoplasm ProteinsNuclear ProteinsTranscription FactorsTranscription, GeneticMLLT1 protein, humanNeoplasm ProteinsNuclear ProteinsTranscription FactorsAcute myeloid leukemia (AML)ENL/MLLT1Epigenetic therapyHematopoiesisHistone acetylationMLL

Identifiers

PMID30066088
PMCPMC11105289
OpenAlexW2886089840

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.