Evidence map›Paper›PMID 7530657›Full record

ArticleThe EMBO journal1995

An acute myeloid leukemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms.

T Tanaka, K Tanaka, S Ogawa, M Kurokawa, K Mitani, J Nishida, Y Shibata, Y Yazaki, H Hirai

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 231 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Glycogen synthase kinase-3 and alternative splicing.Wiley interdisciplinary reviews. RNA · 2018
    Review
  9. RUNX1: A Regulator of NF-kB Signaling in Pulmonary Diseases.Current protein & peptide science · 2018
    Review
  10. Overexpression ofBlood advances · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

12 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.

T TanakaThird Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
K Tanaka
S Ogawa
M Kurokawa
K Mitani
J Nishida
Y Shibata
Y Yazaki
H Hirai
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The AML1 gene on chromosome 21 is disrupted in the (8;21)(q22;q22) and (3;21)(q26;q22) translocations associated with myelogenous leukemias and encodes a DNA binding protein. From the AML1 gene, two representative forms of proteins, AML1a and AML1b, are produced by alternative splicing. Both forms have a DNA binding domain but, unlike AML1b, AML1a lacks a putative transcriptional activation domain. Here we demonstrate that overexpressed AML1a totally suppresses granulocytic differentiation and stimulates cell proliferation in 32Dcl3 murine myeloid cells treated with granulocyte colony-stimulating factor. These effects of AML1a were canceled by the concomitant overexpression of AML1b. Such biological phenomena could be explained by our observations that (i) AML1a, which on its own has no effects as a transcriptional regulator, dominantly suppresses transcriptional activation by AML1b, and (ii) AML1a exhibits the higher affinity for DNA binding compared with AML1b. These antagonistic actions could be important in leukemogenesis and/or myeloid cell differentiation because more than half of myelogenous leukemia patients showed an increase in the relative amounts of AML1a.

Indexed as

Alternative SplicingDNA-Binding ProteinsProto-Oncogene ProteinsAnimalsBone MarrowCore Binding Factor Alpha 2 SubunitGranulocyte Colony-Stimulating FactorHematopoiesisHumansLeukemia, Myeloid, AcuteMiceNeoplasm ProteinsProtein BindingTranscriptional ActivationTranscription FactorsTumor Cells, CulturedCore Binding Factor Alpha 2 SubunitDNA-Binding ProteinsGranulocyte Colony-Stimulating FactorNeoplasm ProteinsProto-Oncogene ProteinsRUNX1 protein, humanRunx1 protein, mousetranscription factor PEA3Transcription Factors

Identifiers

PMID7530657
PMCPMC398088
OpenAlexW15248648

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.