Evidence map›Paper›PMID 7651838›Full record

ArticleNucleic acids research1995

Alternative splicing and genomic structure of the AML1 gene involved in acute myeloid leukemia.

H Miyoshi, M Ohira, K Shimizu, K Mitani, H Hirai, T Imai, K Yokoyama, E Soeda, M Ohki

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Nucleic acids research, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
9.1field-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

107 citing papers in PubMed, 269 citations in OpenAlex.

  1. Trial
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  14. Malignant Transformation InvolvingCell reports. Medicine · 2020
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  19. RUNX1 Dosage in Development and Cancer.Molecules and cells · 2020
    Review
  20. Article

47 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

9 authors at 1 institution in 1 country.

H MiyoshiRadiobiology Division National Cancer Center Research Institute, Tokyo, Japan.
M Ohira
K Shimizu
K Mitani
H Hirai
T Imai
K Yokoyama
E Soeda
M Ohki
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously isolated the AML1 gene, which is rearranged by the t(8;21) translocation in acute myeloid leukemia. The AML1 gene is highly homologous to the Drosophila segmentation gene runt and the mouse transcription factor PEBP2 alpha subunit gene. This region of homology, called the Runt domain, is responsible for DNA-binding and protein--protein interaction. In this study, we isolated and characterized various forms of AML1 cDNAs which reflect a complex pattern of mRNA species. Analysis of these cDNAs has led to the identification of two distinct AML1 proteins, designated AML1b (453 amino acids) and AML1c (480 amino acids), which differ markedly from the previously reported AML1a (250 amino acids) with regard to their C-terminal regions, although all three contain the Runt domain. The large C-terminal region common to AML1b and AML1c is suggested to be a transcriptional activation domain. AML1c differs from AML1b by only 32 amino acids in the N-terminal. Characterization of the genomic structure revealed that the AML1 gene consists of nine exons and spans > 150 kb of genomic DNA. Northern blot analysis demonstrated the presence of six major transcripts, encoding AML1b or AML1c, which can all be explained by the existence of two promoters, alternative splicing and differential usage of three polyadenylation sites. A minor transcript encoding AML1a which results from alternative splicing of a separate exon can be detected only by reverse transcription-polymerase chain reaction amplification. The distinct proteins encoded by the AML1 gene may have different functions, which could contribute to regulating cell growth and/or differentiation through transcriptional regulation of a specific subset of target genes.

Indexed as

DNA-Binding ProteinsOncogenesProto-Oncogene ProteinsAlternative SplicingAmino Acid SequenceAnimalsBase SequenceChromosome MappingChromosomes, Human, Pair 21Chromosomes, Human, Pair 8Cloning, MolecularCore Binding Factor Alpha 2 SubunitDNA, ComplementaryDNA, NeoplasmExonsGene RearrangementCore Binding Factor Alpha 2 SubunitDNA-Binding ProteinsDNA, ComplementaryDNA, NeoplasmNeoplasm ProteinsProto-Oncogene ProteinsRUNX1 protein, humanRunx1 protein, mouseTranscription Factors

Identifiers

PMID7651838
PMCPMC307102
OpenAlexW1980706177

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.