Evidence map›Paper›PMID 7891692›Full record

ArticleMolecular and cellular biology1995

The t(8;21) fusion protein interferes with AML-1B-dependent transcriptional activation.

S Meyers, N Lenny, S W Hiebert

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
16.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

139 citing papers in PubMed, 380 citations in OpenAlex.

  1. Article
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  3. BBA advances · 2022
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  7. RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia.International journal of molecular sciences · 2019
    Review
  8. Review
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  17. Article
  18. The RUNX1-PU.1 axis in the control of hematopoiesis.International journal of hematology · 2015
    Review
  19. Article
  20. Article

79 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

S MeyersDepartment of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105.
N Lenny
S W Hiebert
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Role of AML1-ETO in Acute LeukemiaR01CA064140 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 1994 to 2018
$5.7M
NCI NIH HHS 5 P30 CA 21765NCI NIH HHS R01 CA64140
6 · The paper itself

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.

Indexed as

Proto-Oncogene ProteinsTranscriptional ActivationTranscription, GeneticAlternative SplicingAmino Acid SequenceBase SequenceCell CompartmentationCell NucleusCloning, MolecularConsensus SequenceCore Binding Factor Alpha 2 SubunitCore Binding FactorsDNA-Binding ProteinsDNA, ComplementaryEnhancer Elements, GeneticGene Expression RegulationCore Binding Factor Alpha 2 SubunitCore Binding FactorsDNA-Binding ProteinsDNA, ComplementaryNeoplasm ProteinsProto-Oncogene ProteinsRecombinant Fusion ProteinsRUNX1T1 protein, humanRUNX1 Translocation Partner 1 ProteinTranscription Factors

Identifiers

PMID7891692
PMCPMC230424
OpenAlexW2113086962

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.