Evidence map›Paper›PMID 10082572›Full record

ArticleMolecular and cellular biology1999

HOXA9 forms triple complexes with PBX2 and MEIS1 in myeloid cells.

W F Shen, S Rozenfeld, A Kwong, L G Köm ves, H J Lawrence, C Largman

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

108 citing papers in PubMed, 250 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. MEIS1 and its potential as a cancer therapeutic target (Review).International journal of molecular medicine · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Homeobox gene Meis1 modulates cardiovascular regeneration.Seminars in cell & developmental biology · 2020
    Review
  19. Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020
    Article
  20. Article

48 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

6 authors at 1 institution in 1 country.

W F ShenDepartments of Medicine, University of California VA Medical Center, San Francisco, California, USA. largman@cgl.ucsf.edu
S Rozenfeld
A Kwong
L G Köm ves
H J Lawrence
C Largman
San Francisco VA Medical Center · US

Funding

THE ROLE OF HOX HOMEOBOX GENES IN NORMAL HEMATOPOIESISR01DK048642 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI LAWRENCE, HUGH JEFFREY · 1996 to 2003
$1.0M
NIDDK NIH HHS DK48642NIDDK NIH HHS R01 DK048642
6 · The paper itself

Abstract

Aberrant activation of the HOX, MEIS, and PBX homeodomain protein families is associated with leukemias, and retrovirally driven coexpression of HOXA9 and MEIS1 is sufficient to induce myeloid leukemia in mice. Previous studies have demonstrated that HOX-9 and HOX-10 paralog proteins are unique among HOX homeodomain proteins in their capacity to form in vitro cooperative DNA binding complexes with either the PBX or MEIS protein. Furthermore, PBX and MEIS proteins have been shown to form in vivo heterodimeric DNA binding complexes with each other. We now show that in vitro DNA site selection for MEIS1 in the presence of HOXA9 and PBX yields a consensus PBX-HOXA9 site. MEIS1 enhances in vitro HOXA9-PBX protein complex formation in the absence of DNA and forms a trimeric electrophoretic mobility shift assay (EMSA) complex with these proteins on an oligonucleotide containing a PBX-HOXA9 site. Myeloid cell nuclear extracts produce EMSA complexes which appear to contain HOXA9, PBX2, and MEIS1, while immunoprecipitation of HOXA9 from these extracts results in coprecipitation of PBX2 and MEIS1. In myeloid cells, HOXA9, MEIS1, and PBX2 are all strongly expressed in the nucleus, where a portion of their signals are colocalized within nuclear speckles. However, cotransfection of HOXA9 and PBX2 with or without MEIS1 minimally influences transcription of a reporter gene containing multiple PBX-HOXA9 binding sites. Taken together, these data suggest that in myeloid leukemia cells MEIS1 forms trimeric complexes with PBX and HOXA9, which in turn can bind to consensus PBX-HOXA9 DNA targets.

Indexed as

AnimalsBinding SitesBone Marrow CellsCell NucleusDimerizationHomeodomain ProteinsHumansLeukemia, MyeloidMiceMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsPrecipitin TestsProtein BindingProto-Oncogene ProteinsSubcellular FractionsTranscription Factorshomeobox protein HOXA9Homeodomain ProteinsMEIS1 protein, humanMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsPBX2 protein, humanPbx2 protein, mouseProto-Oncogene ProteinsTranscription Factors

Identifiers

PMID10082572
PMCPMC84099
OpenAlexW2098909302

What OpenQuestion holds

Texttitle and abstract
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.