The t(8;21) Fusion Protein Interferes with AML-1B-Dependent Transcriptional Activation

Meyers, Shari; Lenny, Noel; Hiebert, Scott W.

doi:10.1128/mcb.15.4.1974

Cited by 368Acute Myeloid Leukemia ResearchRetinoids in leukemia and cellular processesGenomics and Chromatin Dynamics

The t(8;21) Fusion Protein Interferes with AML-1B-Dependent Transcriptional Activation

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Meyers, Shari, Lenny, Noel, Hiebert, Scott W.·1995·Molecular and Cellular Biology

DOI 10.1128/mcb.15.4.1974PMC PMC230424

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Abstract

The AML-1/CBF beta transcription factor complex is targeted by both the t(8;21) and the inv(16) chromosomal alterations, which are frequently observed in acute myelogenous leukemia. AML-1 is a site-specific DNA-binding protein that recognizes the enhancer core motif TGTGGT. The t(8;21) translocation fuses the first 177 amino acids of AML-1 to MTG8 (also known as ETO), generating a chimeric protein that retains the DNA-binding domain of AML-1. Analysis of endogenous AML-1 DNA-binding complexes suggested the presence of at least two AML-1 isoforms. Accordingly, we screened a human B-cell cDNA library and isolated a larger, potentially alternatively spliced, form of AML1, termed AML1B. AML-1B is a protein of 53 kDa that binds to a consensus AML-1-binding site and complexes with CBF beta. Subcellular fractionation experiments demonstrated that both AML-1 and AML-1/ETO are efficiently extracted from the nucleus under ionic conditions but that AML-1B is localized to a salt-resistant nuclear compartment. Analysis of the transcriptional activities of AML-1, AML-1B, and AML-1/ETO demonstrated that only AML-1B activates transcription from the T-cell receptor beta enhancer. Mixing experiments indicated that AML-1/ETO can efficiently block AML-1B-dependent transcriptional activation, suggesting that the t(8;21) translocation creates a dominant interfering protein.

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TLE, the Human Homolog of Groucho, Interacts with AML1 and Acts as a Repressor of AML1-Induced Transactivation
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Meyers, S., Lenny, N. T., Sun, W. Y., & Hiebert, S. W. (1996) · PubMed · Cited by 107 · see citing works
Self-citation
The t(12;21) Translocation Converts AML-1B from an Activator to a Repressor of Transcription
Hiebert, S. W., Sun, W., Nathan Davis, J., Golub, T., Shurtleff, S., Buijs, A., Downing, J. R., Grosveld, G., Roussel, M. F., Gary Gilliland, D., et al. (1996) · Molecular and Cellular Biology · doi:10.1128/mcb.16.4.1349 · Cited by 272 · see citing works
Self-citation
Untitled work
(1995) · PubMed · Cited by 198 · see citing works
Self-citation
The AML1 gene: a transcription factor involved in the pathogenesis of myeloid and lymphoid leukemias.
Coco, F. L., Pisegna, S., & Diverio, D. (1997) · PubMed · Cited by 59 · see citing works
Mechanisms of transcriptional repression by the t(8;21)-, t(12;21)-, and inv(16)-encoded fusion proteins
Hiebert, S. W., Lutterbach, B. A., Durst, K. L., Wang, L., Linggi, B. E., Wu, S. W., Wood, L. D., Amann, J. M., King, D., & Hou, Y. (2001) · Cancer Chemotherapy and Pharmacology · doi:10.1007/s002800100302 · Cited by 30 · see citing works
Self-citation

Authors: Meyers, S., Lenny, N., & Hiebert, S. W.
Affiliations: St. Jude Children's Research Hospital (US)
ORCID: Hiebert, Scott W.
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 1995-04-01
Volume: 15
Issue: 4
Pages: 1974-1982
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.15.4.1974
PMC: PMC230424
OpenAlex: W2113086962
Cited by: 368
References: 46
Citations by year: 2025: 1 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 5 · 2015: 8 · 2014: 4 · 2013: 11 · 2012: 3
FWCI: 18.34
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Molecular and Cellular Biology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: American Lebanese Syrian Associated Charities
National Institutes of Health
National Cancer Institute (R01CA064140, P30CA021765)
Topics: Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: ETO, CBFβ, acute myeloid leukemia, transcriptional activation, alternative splicing, DNA-binding domain, nuclear localization, chromosomal translocation
MeSH terms: RUNX1 Translocation Partner 1 Protein, Amino Acid Sequence, Base Sequence, Cell Compartmentation, Cell Nucleus, Cloning, Molecular, DNA-Binding Proteins, Enhancer Elements, Genetic, Gene Expression Regulation, Molecular Sequence Data, Neoplasm Proteins, Protein Binding, Proto-Oncogene Proteins, Recombinant Fusion Proteins, Transcription Factors, Transcription, Genetic, Leukemia, Myeloid, Acute, Transcriptional Activation, Consensus Sequence, Alternative Splicing, DNA, Complementary, Core Binding Factors, Core Binding Factor Alpha 2 Subunit

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The t(8;21) Fusion Protein Interferes with AML-1B-Dependent Transcriptional Activation

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