Evidence map›Paper›PMID 16525506›Full record

ArticleThe EMBO journal2006

TGFbeta/BMP inhibits the bone marrow transformation capability of Hoxa9 by repressing its DNA-binding ability.

Ning Wang, Hyung-Gyoong Kim, Claudiu V Cotta, Mei Wan, Yi Tang, Christopher A Klug, Xu Cao

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. BMP signaling in cancer stemness and differentiation.Cell regeneration (London, England) · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Targeting self-renewal pathways in myeloid malignancies.Cell communication and signaling : CCS · 2013
    Article
  10. Structural basis for homeodomain recognition by the cell-cycle regulator Geminin.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Hox specificity unique roles for cofactors and collaborators.Current topics in developmental biology · 2009
    Review
  18. Cross-regulatory protein-protein interactions between Hox and Pax transcription factors.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  19. Article
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

7 authors at 1 institution in 1 country.

Ning WangDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Hyung-Gyoong Kim
Claudiu V Cotta
Mei Wan
Yi Tang
Christopher A Klug
Xu Cao
University of Alabama at Birmingham · US

Funding

Smad6/7 as Sex Steroid Hormone Receptor CorepressorsR01DK060913 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CAO, XU · 2002 to 2005
$1.0M
NIDDK NIH HHS DK60913NIDDK NIH HHS R01 DK060913
6 · The paper itself

Abstract

Homeobox (Hox) gene mutations and their altered expressions are frequently linked to human leukemia. Here, we report that transforming growth factor beta (TGFbeta)/bone morphogenetic protein (BMP) inhibits the bone marrow transformation capability of Hoxa9 and Nup98-Hoxa9, the chimeric fusion form of Hoxa9 identified in human acute myeloid leukemia (AML), through Smad4, the common Smad (Co-Smad) in the TGFbeta/BMP signaling pathway. Smad4 interacts directly with the homeodomain of Hoxa9 and blocks the ability of Nup98-Hoxa9 to bind DNA, thereby suppressing its ability to regulate downstream gene transcription. Mapping data revealed that the amino-terminus of Smad4 mediates this interaction and overexpression of the Hoxa9 interaction domain of Smad4 was sufficient to inhibit the enhanced serial replating ability of primary bone marrow cells induced by Nup98-Hoxa9. These studies establish a novel mechanism by which TGFbeta/BMP regulates hematopoiesis and suggest that modification of Hox DNA-binding activity may serve as a novel therapeutic intervention for those leukemias that involve deregulation of Hox.

Indexed as

Cell Transformation, NeoplasticAnimalsBone Marrow CellsBone Morphogenetic ProteinsCells, CulturedDNA-Binding ProteinsHematopoiesisHomeodomain ProteinsMiceMutationNuclear Pore Complex ProteinsOncogene Proteins, FusionProtein BindingProtein Structure, TertiarySignal TransductionSmad4 ProteinBone Morphogenetic ProteinsDNA-Binding Proteinshomeobox protein HOXA9Homeodomain Proteinsnuclear pore complex protein 98Nuclear Pore Complex ProteinsOncogene Proteins, FusionSmad4 ProteinSmad4 protein, mouseTransforming Growth Factor beta

Identifiers

PMID16525506
PMCPMC1440313
OpenAlexW1979615853

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.