Evidence map›Paper›PMID 38889007›Full record

ArticleCell reports2024

An enhancer RNA recruits KMT2A to regulate transcription of Myb.

Juhyun Kim, Luis F Diaz, Matthew J Miller, Benjamin Leadem, Ivan Krivega, Ann Dean

Abstract read
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Direct roles of long non-coding RNAs in transcription activation.Nature structural & molecular biology · 2026
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  6. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Juhyun KimLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: juhyun.kim@nih.gov.
Luis F DiazLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA; Oregon Health and Sciences University, Portland, OR 97239, USA.
Matthew J MillerLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA; University of Iowa Medical School, Iowa City, IA 52242, USA.
Benjamin LeademLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA; GeneDx, Gaithersburg, MD 20877, USA.
Ivan KrivegaLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA; Sonothera, South San Francisco, CA 94080, USA.
Ann DeanLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: ann.dean@nih.gov.

Funding

Epigenetic and Developmental Regulation of Mammalian GenesZIADK075033 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DEAN, ANN · 2009 to 2025
$24.2M
Intramural NIH HHS ZIA DK075033
6 · The paper itself

Abstract

The Myb proto-oncogene encodes the transcription factor c-MYB, which is critical for hematopoiesis. Distant enhancers of Myb form a hub of interactions with the Myb promoter. We identified a long non-coding RNA (Myrlin) originating from the -81-kb murine Myb enhancer. Myrlin and Myb are coordinately regulated during erythroid differentiation. Myrlin TSS deletion using CRISPR-Cas9 reduced Myrlin and Myb expression and LDB1 complex occupancy at the Myb enhancers, compromising enhancer contacts and reducing RNA Pol II occupancy in the locus. In contrast, CRISPRi silencing of Myrlin left LDB1 and the Myb enhancer hub unperturbed, although Myrlin and Myb expressions were downregulated, decoupling transcription and chromatin looping. Myrlin interacts with the KMT2A/MLL1 complex. Myrlin CRISPRi compromised KMT2A occupancy in the Myb locus, decreasing CDK9 and RNA Pol II binding and resulting in Pol II pausing in the Myb first exon/intron. Thus, Myrlin directly participates in activating Myb transcription by recruiting KMT2A.

Indexed as

Enhancer Elements, GeneticHistone-Lysine N-MethyltransferaseMyeloid-Lymphoid Leukemia ProteinProto-Oncogene Proteins c-mybTranscription, GeneticAnimalsCell DifferentiationCyclin-Dependent Kinase 9Enhancer RNAsHumansMiceProtein BindingProto-Oncogene MasRNA, Long NoncodingRNA Polymerase IICyclin-Dependent Kinase 9Enhancer RNAsHistone-Lysine N-MethyltransferaseKmt2a protein, mouseMAS1 protein, humanMyeloid-Lymphoid Leukemia ProteinProto-Oncogene MasProto-Oncogene Proteins c-mybRNA, Long NoncodingRNA Polymerase IICP: Molecular biologyenhancer hubenhancer RNAerythroid differentiationgene expressionH3K4me3KMT2AlncRNAMLL1MybPol II pause release

Identifiers

PMID38889007
PMCPMC11369905

What OpenQuestion holds

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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.