Evidence map›Paper›PMID 19158279›Full record

ArticleMolecular and cellular biology2009

Phosphorylation of Fli1 at threonine 312 by protein kinase C delta promotes its interaction with p300/CREB-binding protein-associated factor and subsequent acetylation in response to transforming growth factor beta.

Yoshihide Asano, Maria Trojanowska

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Fli1 and Tissue Fibrosis in Various Diseases.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. What can we learn fromJournal of scleroderma and related disorders · 2018
    Review
  13. Article
  14. Article
  15. Review
  16. Vasculopathy in scleroderma.Seminars in immunopathology · 2015
    Review
  17. Article
  18. Review
  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

2 authors at 1 institution in 1 country.

Yoshihide AsanoDivision of Rheumatology and Immunology, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Maria Trojanowska
Medical University of South Carolina · US

Funding

THE ROLE OF FLI1 IN CELLULAR DIFFERENTIATION AND DEVELOPMENTP01CA078582 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2009
$9.1M
The molecular mechanisms of fibrosisR01AR042334 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1994 to 2018
$5.2M
NCI NIH HHS P01 CA078582NCI NIH HHS P01 CA78582NIAMS NIH HHS AR042334NIAMS NIH HHS R01 AR042334
6 · The paper itself

Abstract

Previous studies have shown that transforming growth factor beta (TGF-beta)-induced collagen gene expression involves acetylation-dependent dissociation from the human alpha2(I) collagen (COL1A2) promoter of the transcriptional repressor Fli1. The goal of this study was to elucidate the regulatory steps preceding the acetylation of Fli1. We first showed that TGF-beta induces Fli1 phosphorylation on a threonine residue(s). The major phosphorylation site was localized to threonine 312 located in the DNA binding domain of Fli1. Using several independent approaches, we demonstrated that Fli1 is directly phosphorylated by protein kinase C delta (PKC delta). Additional experiments showed that in response to TGF-beta, PKC delta is recruited to the collagen promoter to phosphorylate Fli1 and that this step is a prerequisite for the subsequent interaction of Fli1 with p300/CREB-binding protein-associated factor (PCAF) and an acetylation event. The phosphorylation of endogenous Fli1 preceded its acetylation in response to TGF-beta stimulation, and the blockade of PKC delta abrogated both the phosphorylation and acetylation of Fli1 in dermal fibroblasts. Promoter studies showed that a phosphorylation-deficient mutant of Fli1 exhibited an increased inhibitory effect on the COL1A2 gene, which could not be reversed by the forced expression of PCAF or PKC delta. These data strongly suggest that the phosphorylation-acetylation cascade triggered by PKC delta represents the primary mechanism whereby TGF-beta regulates the transcriptional activity of Fli1 in the context of the collagen promoter.

Indexed as

AcetylationCells, CulturedCollagenCollagen Type IDermisFibroblastsHumansInfant, NewbornMalep300-CBP-Associated Factorp300-CBP Transcription FactorsPhosphorylationPhosphothreoninePromoter Regions, GeneticProtein BindingProtein Kinase C-deltaCollagenCollagen Type IFLI1 protein, humanp300-CBP-Associated Factorp300-CBP Transcription FactorsPhosphothreonineProtein Kinase C-deltaProto-Oncogene Protein c-fli-1Smad ProteinsTransforming Growth Factor beta

Identifiers

PMID19158279
PMCPMC2655609
OpenAlexW2099082723

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.