Evidence map›Paper›PMID 14966289›Full record

ArticleMolecular and cellular biology2004

Developmentally essential protein flightless I is a nuclear receptor coactivator with actin binding activity.

Young-Ho Lee, Hugh D Campbell, Michael R Stallcup

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

65 citing papers in PubMed, 130 citations in OpenAlex.

  1. Review
  2. Review
  3. mSphere · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Overexpression ofInternational journal of molecular sciences · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. ArabidopsisPlant physiology · 2018
    Article
  16. Article
  17. Flightless-I Controls Fat Storage inMolecules and cells · 2018
    Article
  18. Article
  19. Article
  20. Article

5 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

3 authors at 2 institutions in 2 countries.

Young-Ho LeeDepartment of Pathology, University of Southern California, Los Angeles, California 90089-9092, USA.
Hugh D Campbell
Michael R Stallcup
Australian National University · AUUniversity of Southern California · US

Funding

Transcription activation by nuclear coactivatorsR01DK043093 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STALLCUP, MICHAEL R · 1990 to 2019
$6.5M
NIDDK NIH HHS DK43093NIDDK NIH HHS R01 DK043093
6 · The paper itself

Abstract

Hormone-activated nuclear receptors (NR) activate transcription by recruiting multiple coactivator complexes to the promoters of target genes. One important coactivator complex includes a p160 coactivator (e.g., GRIP1, SRC-1, or ACTR) that binds directly to activated NR, the histone acetyltransferase p300 or CBP, and the arginine-specific histone methyltransferase CARM1. We previously demonstrated that the coactivator function of CARM1 depends both on the methyltransferase activity and on additional unknown proteins that bind to CARM1. In this study a yeast two-hybrid screen for proteins that bind CARM1 identified the protein Flightless I (Fli-I), which has essential roles in Drosophila and mouse development. Fli-I bound to CARM1, GRIP1, and NRs and cooperated synergistically with CARM1 and GRIP1 to enhance NR function. Fli-I bound poorly to and did not cooperate with PRMT1, a CARM1-related protein arginine methyltransferase that also functions as an NR coactivator. The synergy between GRIP1, CARM1, and Fli-I required the methyltransferase activity of CARM1. The C-terminal AD1 (binding site for p300/CBP) and AD2 (binding site for CARM1) activation domains of GRIP1 contributed to the synergy but were less stringently required than the N-terminal region of GRIP1, which is the binding site for Fli-I. Endogenous Fli-I was recruited to the estrogen-regulated pS2 gene promoter of MCF-7 cells in response to the hormone, and reduction of endogenous Fli-I levels by small interfering RNA reduced hormone-stimulated gene expression by the endogenous estrogen receptor. A fragment of Fli-I that is related to the actin binding protein gelsolin enhanced estrogen receptor activity, and mutations that reduced actin binding also reduced the coactivator function of this Fli-I fragment. These data suggest that Fli-I may facilitate interaction of the p160 coactivator complex with other coactivators or coactivator complexes containing actin or actin-like proteins.

Indexed as

Drosophila ProteinsGelsolinActinsAdaptor Proteins, Signal TransducingAnimalsCarrier ProteinsCell Line, TumorEstradiolGenes, ReporterHumansMacromolecular SubstancesMembrane ProteinsMiceMicrofilament ProteinsNerve Tissue ProteinsNuclear ProteinsActinsAdaptor Proteins, Signal TransducingCarrier Proteinscoactivator-associated arginine methyltransferase 1Drosophila ProteinsEstradiolFLII protein, humanGelsolinGRIP1 protein, humanGrip1 protein, mouseGrip protein, DrosophilaMacromolecular SubstancesMembrane ProteinsMicrofilament ProteinsNerve Tissue ProteinsNuclear ProteinsProtein-Arginine N-MethyltransferasesReceptors, AMPAReceptors, Cytoplasmic and NuclearRecombinant Fusion ProteinsRNA, Small InterferingTrans-Activators

Identifiers

PMID14966289
PMCPMC350567
OpenAlexW2106110723

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.