Evidence map›Paper›PMID 10611307›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

The t(8;21) chromosomal translocation in acute myelogenous leukemia modifies intranuclear targeting of the AML1/CBFalpha2 transcription factor.

S McNeil, C Zeng, K S Harrington, S Hiebert, J B Lian, J L Stein, A J van Wijnen, G S Stein

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Bookmarking the genome: maintenance of epigenetic information.The Journal of biological chemistry · 2011
    Review
  10. An architectural genetic and epigenetic perspective.Integrative biology : quantitative biosciences from nano to macro · 2011
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Transcription-factor-mediated epigenetic control of cell fate and lineage commitment.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2009
    Review
  18. Article
  19. Article
  20. Review
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

8 authors at 2 institutions in 1 country.

S McNeilDepartment of Cell Biology, University of Massachusetts, Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.
C Zeng
K S Harrington
S Hiebert
J B Lian
J L Stein
A J van Wijnen
G S Stein
University of Massachusetts Chan Medical School · USVanderbilt University · US

Funding

NUCLEAR MATRIX MEDIATED TRANSCRIPTIONAL CONTROL OF OSTEOBLAST GENE EXPRESSIONR01AR045688 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STEIN, GARY S. · 1998 to 2001
$922k
PROGRAM PROJECT--STEM CELL BIOLOGYP01DK050222 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KITTLER, ELLEN L · 1996 to 1999
–
NIAMS NIH HHS AR45688NIDDK NIH HHS DK50222
6 · The paper itself

Abstract

Targeting of gene regulatory factors to specific intranuclear sites may be critical for the accurate control of gene expression. The acute myelogenous leukemia 8;21 (AML1/ETO) fusion protein is encoded by a rearranged gene created by the ETO chromosomal translocation. This protein lacks the nuclear matrix-targeting signal that directs the AML1 protein to appropriate gene regulatory sites within the nucleus. Here we report that substitution of the chromosome 8-derived ETO protein for the multifunctional C terminus of AML1 precludes targeting of the factor to AML1 subnuclear domains. Instead, the AML1/ETO fusion protein is redirected by the ETO component to alternate nuclear matrix-associated foci. Our results link the ETO chromosomal translocation in AML with modifications in the intranuclear trafficking of the key hematopoietic regulatory factor, AML1. We conclude that misrouting of gene regulatory factors as a consequence of chromosomal translocations is an important characteristic of acute leukemias.

Indexed as

DNA-Binding ProteinsProto-Oncogene ProteinsBiological TransportCell CompartmentationCell NucleusCore Binding Factor Alpha 2 SubunitHumansLeukemia, Myeloid, AcuteNuclear Localization SignalsNuclear MatrixOncogene Proteins, FusionRUNX1 Translocation Partner 1 ProteinTranscription FactorsTranslocation, GeneticAML1-ETO fusion protein, humanCore Binding Factor Alpha 2 SubunitDNA-Binding ProteinsNuclear Localization SignalsOncogene Proteins, FusionProto-Oncogene ProteinsRUNX1 protein, humanRUNX1 Translocation Partner 1 ProteinTranscription Factors

Identifiers

PMID10611307
PMCPMC24742
OpenAlexW2099941735

What Socratic 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 Socratic graph.