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

The t(8;21) Fusion Product, AML-1–ETO, Associates with C/EBP-α, Inhibits C/EBP-α-Dependent Transcription, and Blocks Granulocytic Differentiation

1 Jan 1998

Abstract excerpt

AML-1B is a hematopoietic transcription factor that is functionally inactivated by multiple chromosomal translocations in human acute myeloblastic and B-cell lymphocytic leukemias. The t(8;21)(q22;q22) translocation replaces the C terminus, including the transactivation domain of AML-1B, with ETO, a nuclear protein of unknown function. We previously showed that AML-1-ETO is a dominant inhibitor of...

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 Chronic Lymphocytic Leukemia Research
Share to Immune Cell Function and Interaction

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 9418879
DOI: 10.1128/mcb.18.1.322

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The t(8;21) Fusion Product, AML-1–ETO, Associates with C/EBP-α, Inhibits C/EBP-α-Dependent Transcription, and Blocks Granulocytic DifferentiationPMID 9418879Read ↗

The t(8;21) Fusion Protein Interferes with AML-1B-Dependent Transcriptional ActivationSemantic proximity Read ↗

C/EBPα overrides epigenetic reprogramming by oncogenic transcription factors in acute myeloid leukemia.Semantic proximity Read ↗

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

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

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

The AML1/ETO fusion protein activates transcription of BCL-2Semantic proximity Read ↗

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

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

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

Inhibition of the Transforming Growth Factor β1 Signaling Pathway by the AML1/ETO Leukemia-associated Fusion ProteinSemantic proximity Read ↗

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

p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced deathSemantic proximity Read ↗

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