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

ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex

1 Sept 1998

Abstract excerpt

The t(8;21) translocation between two genes known as AML1 and ETO is seen in approximately 12-15% of all acute myeloid leukemia (AML) and is the second-most-frequently observed nonrandom genetic alteration associated with AML. AML1 up-regulates a number of target genes critical to normal hematopoiesis, whereas the AML1/ETO fusion interferes with this trans-activation. We discovered that the fusion partner ETO...

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 Histone Deacetylase Inhibitors Research
Share to Retinoids in leukemia and cellular processes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 9724795
DOI: 10.1073/pnas.95.18.10860

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complexPMID 9724795Read ↗

Domains involved in ETO and human N-CoR interaction and ETO transcription repression.Semantic proximity Read ↗

The nuclear receptor co-repressor (N-CoR) utilizes repression domains I and III for interaction and co-repression with ETO.Semantic proximity Read ↗

t(8;21) Acute Myeloid Leukemia as a Paradigm for the Understanding of Leukemogenesis at the Level of Gene Regulation and Chromatin Programming.Semantic proximity Read ↗

Multiple subnuclear targeting signals of the leukemia-related AML1/ETO and ETO repressor proteinsSemantic proximity Read ↗

RUNX1-ETO: Attacking the Epigenome for Genomic Instable LeukemiaSemantic proximity Read ↗

ETO protein of t(8;21) AML is a corepressor for Bcl-6 B-cell lymphoma oncoproteinSemantic proximity Read ↗

Disruption of the NHR4 domain structure in AML1-ETO abrogates SON binding and promotes leukemogenesisSemantic proximity Read ↗

An AML1-ETO/miR-29b-1 regulatory circuit modulates phenotypic properties of acute myeloid leukemia cells.Semantic proximity Read ↗

MEIS2 Is an Oncogenic Partner in AML1-ETO-Positive AMLSemantic proximity Read ↗

AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches.Semantic proximity Read ↗

Structural basis for recognition of SMRT/N-CoR by the MYND domain and its contribution to AML1/ETO's activity.Semantic proximity Read ↗

RUNX1/AML1 DNA-binding domain and ETO/MTG8 NHR2-dimerization domain are critical to AML1-ETO9a leukemogenesisSemantic proximity Read ↗

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