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

A Mechanism of Repression by Acute Myeloid Leukemia-1, the Target of Multiple Chromosomal Translocations in Acute Leukemia

1 Jan 2000

Abstract excerpt

AML1 is one of the most frequently translocated genes in human leukemia. Here we demonstrate that acute myeloid leukemia-1 (AML-1) (Runx-1) represses transcription from a native promoter, p21(Waf1/Cip1). Unexpectedly, this repression did not require interactions with the Groucho co-repressor. To define the mechanism of repression, we asked whether other co-repressors could interact with AML-1. We demonstrate that...

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 Genomics and Chromatin Dynamics
Share to RNA Research and Splicing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 10617663
DOI: 10.1074/jbc.275.1.651

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A Mechanism of Repression by Acute Myeloid Leukemia-1, the Target of Multiple Chromosomal Translocations in Acute LeukemiaPMID 10617663Read ↗

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

Transcriptional repression of the RUNX3/AML2 gene by the t(8;21) and inv(16) fusion proteins in acute myeloid leukemiaSemantic proximity Read ↗

Runx1 regulation of Pu.1 corepressor/coactivator exchange identifies specific molecular targets for leukemia differentiation therapy.Semantic proximity Read ↗

Transcription factor RUNX1 promotes survival of acute myeloid leukemia cellsSemantic proximity Read ↗

Addiction of t(8;21) and inv(16) Acute Myeloid Leukemia to Native RUNX1Semantic proximity Read ↗

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

Transcriptional upregulation of p21/WAF/Cip1 in myeloid leukemic blasts expressing AML1-ETO.Semantic proximity Read ↗

RUNX1 Is a Key Target in t(4;11) Leukemias that Contributes to Gene Activation through an AF4-MLL Complex InteractionSemantic proximity Read ↗

Gatekeeper function of the RUNX1 transcription factor in acute leukemia.Semantic proximity Read ↗

AML1/RUNX1 functions as a cytoplasmic attenuator of NF-κB signaling in the repression of myeloid tumors.Semantic proximity Read ↗

The Runx-PU.1 pathway preserves normal and AML/ETO9a leukemic stem cells.Semantic proximity Read ↗

Activation of AML1‐mediated transcription by MOZ and inhibition by the MOZ–CBP fusion proteinSemantic proximity Read ↗

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