Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Degree of Recruitment of DOT1L to MLL-AF9 Defines Level of H3K79 Di- and Tri-methylation on Target Genes and Transformation Potential

25 Apr 2015

Abstract excerpt

The MLL gene is a common target of chromosomal translocations found in human leukemia. MLL-fusion leukemia has a consistently poor outcome. One of the most common translocation partners is AF9 (MLLT3). MLL-AF9 recruits DOT1L, a histone 3 lysine 79 methyltransferase (H3K79me1/me2/me3), leading to aberrant gene transcription. We show that DOT1L has three AF9 binding sites and present the nuclear magnetic resonance...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acute Myeloid Leukemia Research
Share to Cancer-related gene regulation
Share to Epigenetics and DNA Methylation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 25921540
DOI: 10.1016/j.celrep.2015.04.004

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Degree of Recruitment of DOT1L to MLL-AF9 Defines Level of H3K79 Di- and Tri-methylation on Target Genes and Transformation PotentialPMID 25921540Read ↗

MLL-fusion-driven leukemia requires SETD2 to safeguard genomic integritySemantic proximity Read ↗

Targeting Recruitment of Disruptor of Telomeric Silencing 1-like (DOT1L)Semantic proximity Read ↗

hDOT1L Links Histone Methylation to LeukemogenesisSemantic proximity Read ↗

Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1lSemantic proximity Read ↗

AF10 (MLLT10) prevents somatic cell reprogramming through regulation of DOT1L-mediated H3K79 methylationSemantic proximity Read ↗

Histone H3 Lysine 79 Methyltransferase Dot1 Is Required for Immortalization by MLL OncogenesSemantic proximity Read ↗

SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformationSemantic proximity Read ↗

The Intrinsically Disordered Proteins MLLT3 (AF9) and MLLT1 (ENL) - Multimodal Transcriptional Switches With Roles in Normal Hematopoiesis, MLL Fusion Leukemia, and Kidney Cancer.Semantic proximity Read ↗

DOT1L interaction partner AF10 controls patterning of H3K79 methylation and RNA polymerase II to maintain cell identitySemantic proximity Read ↗

DOT1L Complex Regulates Transcriptional Initiation in Human CellsSemantic proximity Read ↗

MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genomeSemantic proximity Read ↗

Histone H2B ubiquitin ligase RNF20 is required for <i>MLL</i> -rearranged leukemiaSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.