Evidence map›Paper›PMID 10698505›Full record

ArticleOncogene2000

HoxA9-mediated immortalization of myeloid progenitors requires functional interactions with TALE cofactors Pbx and Meis.

C A Schnabel, Y Jacobs, M L Cleary

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

60 citing papers in PubMed, 132 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Inhibition of non-small-cell lung cancer cell proliferation by Pbx1.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2014
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

C A SchnabelDepartment of Pathology, Stanford University School of Medicine, California 94305, USA.
Y Jacobs
M L Cleary
Stanford University · US

Funding

TUMOR BIOLOGYT32CA009151 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1985 to 2014
$5.5M
MOLECULAR PATHOLOGY OF LYMPHOID MALIGNANCIESR37CA042971 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1999 to 2006
$3.6M
MOLECULAR PATHOLOGY OF LYMPHOID MALIGNANCIESR01CA042971 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1986 to 1998
–
NCI NIH HHS CA09151NCI NIH HHS CA42971NIAID NIH HHS AI-07290
6 · The paper itself

Abstract

Specific Hox genes are implicated in leukemic transformation, and their selective genetic collaboration with TALE homeobox genes, Pbx and Meis, accentuates their oncogenic potential. The molecular mechanisms underlying these coordinate functions, however, have not been characterized. In this study, we demonstrate that HoxA9 requires its Pbx interaction motif as well as its amino terminus to enhance the clonogenic potential of myeloid progenitors in vitro. We further show that HoxA9 forms functional trimeric DNA binding complexes with Pbx and Meis-like proteins on a modified enhancer. DNA binding complexes containing HoxA9 and TALE homeoproteins display cooperative transcriptional activity and are present in leukemic cells. Trimeric complex formation on its own, however, is not sufficient for HoxA9-mediated immortalization. Rather, structure-function analyses demonstrate that domains of HoxA9 which are necessary for cellular transformation are coincident with those required for trimer-mediated transcriptional activation. Furthermore, the amino terminus of HoxA9 provides essential transcriptional effector properties and its requirement for myeloid transformation can be functionally replaced by the VP16 activation domain. These data suggest that biochemical interactions between HoxA9 and TALE homeoproteins mediate cellular transformation in hematopoietic cells, and that their transcriptional activity in higher order DNA binding complexes provides a molecular basis for their collaborative roles in leukemogenesis.

Indexed as

Repressor ProteinsAmino Acid MotifsAnimalsBiopolymersCell DivisionCell LineCell Line, TransformedCell Transformation, NeoplasticDNA-Binding ProteinsHematopoietic Stem CellsHomeodomain ProteinsLeukemia, MyeloidMiceMice, Inbred C57BLMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsBiopolymersDNA-Binding Proteinshomeobox protein HOXA9Homeodomain ProteinsMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsPbx2 protein, mouseProto-Oncogene ProteinsRepressor ProteinsTgif1 protein, mouse

Identifiers

PMID10698505
OpenAlexW2317471234

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.