Evidence map›Paper›PMID 11592991›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Segmentation gene product Fushi tarazu is an LXXLL motif-dependent coactivator for orphan receptor FTZ-F1.

T Suzuki, H Kawasaki, R T Yu, H Ueda, K Umesono

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

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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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Variation and constraint in Hox gene evolution.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  4. Article
  5. Article
  6. Surprising flexibility in a conserved Hox transcription factor over 550 million years of evolution.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  7. Article
  8. Article
  9. 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

5 authors.

T SuzukiInstitute for Virus Research, and Graduate School for Biostudies, Kyoto University, Kyoto 606-8507, Japan.
H Kawasaki
R T Yu
H Ueda
K Umesono

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Orphan receptors for whom cognate ligands have not yet been identified form a large subclass within the nuclear receptor superfamily. To address one aspect of how they might regulate transcription, we analyzed the mode of interaction between the Drosophila orphan receptor FTZ-F1 (NR5A3) and a segmentation gene product Fushi tarazu (FTZ). Strong interaction between these two factors was detected by use of the mammalian one- and two-hybrid interaction assays without addition of ligand. This interaction required the AF-2 core and putative ligand-binding domain of FTZ-F1 and the LXXLL motif of FTZ. The requirement of these elements was further confirmed by examination of their target gene expression in Drosophila embryos and observation of a cuticle phenotype in transgenic fly lines that express mutated factors. In Drosophila cultured cells, FTZ is required for FTZ-F1 activation of a FTZ-F1 reporter gene. These results reveal a resemblance in the mode of interaction between FTZ-F1 and FTZ and that of nuclear receptor-coactivator and indicate that direct interaction is required for regulation of gene expression by FTZ-F1. Thus, we propose that FTZ may represent a category of LXXLL motif-dependent coactivators for nuclear receptors.

Indexed as

Amino Acid MotifsAmino Acid SequenceAnimalsBinding SitesCells, CulturedDNA-Binding ProteinsDrosophilaDrosophila ProteinsFushi Tarazu Transcription FactorsHomeodomain ProteinsInsect ProteinsMolecular Sequence DataReceptors, Cytoplasmic and NuclearSteroidogenic Factor 1Transcription FactorsDNA-Binding ProteinsDrosophila Proteinsftz protein, DrosophilaFushi Tarazu Transcription FactorsHomeodomain ProteinsInsect Proteinsnuclear hormone receptor FTZ-F1, DrosophilaReceptors, Cytoplasmic and NuclearSteroidogenic Factor 1Transcription Factors

Identifiers

PMID11592991
PMCPMC60066

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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.