Evidence map›Paper›PMID 20553494›Full record

ArticleThe FEBS journal2010

An autoinhibitory effect of the homothorax domain of Meis2.

Cathy Hyman-Walsh, Glen A Bjerke, David Wotton

Open access · bronzeAbstract read
In one paragraph

Article in The FEBS journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Hippo Signaling in Cancer: Lessons FromFrontiers in cell and developmental biology · 2019
    Review
  10. Article
  11. Article
  12. Depletion of MEIS2 inhibits osteogenic differentiation potential of human dental stem cells.International journal of clinical and experimental medicine · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. 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.

Cathy Hyman-WalshDepartment of Biochemistry and Molecular Genetics, and Center for Cell Signaling, University of Virginia, Charlottesville, VA, USA.
Glen A Bjerke
David Wotton
University of Virginia · US

Funding

UVA Digestive Health Research CenterP30DK067629 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI PIZARRO, THERESA TORRES · 2004 to 2008
$5.6M
MOLECULAR ANALYSIS OF TRANSCRIPTIONAL REPRESSION BY TGIFR01HD039926 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI WOTTON, DAVID · 2001 to 2010
$2.5M
NICHD NIH HHS R01 HD039926NIDDK NIH HHS P30 DK067629
6 · The paper itself

Abstract

Myeloid ecotropic insertion site (Meis)2 is a homeodomain protein containing a conserved homothorax (Hth) domain that is present in all Meis and Prep family proteins and in the Drosophila Hth protein. The Hth domain mediates interaction with Pbx homeodomain proteins, allowing for efficient DNA binding. Here we show that, like Meis1, Meis2 has a strong C-terminal transcriptional activation domain, which is required for full activation of transcription by homeodomain protein complexes composed of Meis2 and Pbx1. We also show that the activity of the activation domain is inhibited by the Hth domain, and that this autoinhibition can be partially relieved by the interaction of Pbx1 with the Hth domain of Meis2. Targeting of the Hth domain to DNA suggests that it is not a portable trans-acting repression domain. However, the Hth domain can inhibit a linked activation domain, and this inhibition is not limited to the Meis2 activation domain. Database searching reveals that the Meis3.2 splice variant, which is found in several vertebrate species, disrupts the Hth domain by removing 17 codons from the 5'-end of exon 6. We show that the equivalent deletion in Meis2 derepresses the C-terminal activation domain and weakens interaction with Pbx1. This work suggests that the transcriptional activity of all members of the Meis/Prep Hth protein family is subject to autoinhibition by their Hth domains, and that the Meis3.2 splice variant encodes a protein that bypasses this autoinhibitory effect.

Indexed as

Alternative SplicingAmino Acid SequenceAnimalsCell Line, TumorDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsHomeodomain ProteinsHumansMiceMolecular Sequence DataPre-B-Cell Leukemia Transcription Factor 1Protein Structure, TertiaryProto-Oncogene ProteinsSequence AlignmentTranscriptional ActivationDNA-Binding ProteinsDrosophila ProteinsHomeodomain Proteinshth protein, DrosophilaMEIS2 protein, humanPBX1 protein, humanPre-B-Cell Leukemia Transcription Factor 1Proto-Oncogene ProteinsTranscription Factors

Identifiers

PMID20553494
PMCPMC4306237
OpenAlexW1642411512

What OpenQuestion holds

Textmetadata
LicenceTDM
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.