Evidence map›Paper›PMID 15750622›Full record

ArticleOncogene2005

Selective inhibition of TGF-beta responsive genes by Smad-interacting peptide aptamers from FoxH1, Lef1 and CBP.

Qiqi Cui, Sang Kyun Lim, Bryan Zhao, Francis Michael Hoffmann

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Cancers · 2021
    Article
  6. Article
  7. Review
  8. Transforming growth factor-β: A therapeutic target for cancer.Human vaccines & immunotherapeutics · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Alterations in the Smad pathway in human cancers.Frontiers in bioscience (Landmark edition) · 2012
    Review
  15. TGF-β in the Bone Microenvironment: Role in Breast Cancer Metastases.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2011
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

4 authors at 1 institution in 1 country.

Qiqi CuiMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA.
Sang Kyun Lim
Bryan Zhao
Francis Michael Hoffmann
University of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Training in Cancer Biology Training GrantT32CA009135 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SUGDEN, WILLIAM M. · 1985 to 2024
$10.4M
Chemical Genetics of TGF-Beta Signal TransductionR01CA090875 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI HOFFMANN, F. MICHAEL · 2002 to 2006
$1.3M
E M Transdifferentiation in Proximal Tubule CellsR21DK064336 · NIDDK · UNIVERSITY OF WISCONSIN MADISON · PI BECKER, BRYAN N · 2003 to 2004
$291k
NCI NIH HHS P30 CA 014520NCI NIH HHS R01 CA 090875NCI NIH HHS T32 CA 09135NIDDK NIH HHS R21 DK 064336
6 · The paper itself

Abstract

Transforming growth factor beta (TGF-beta) stimulation results in the assembly of Smad-containing protein complexes that mediate activation or repression of TGF-beta responsive genes. To determine if disruption of specific Smad protein-protein interactions would selectively inhibit responses to TGF-beta or generally interfere with Smad-dependent signaling, we developed three Smad-binding peptide aptamers by introducing Smad interaction motifs from Smad-binding proteins CBP, FoxH1 and Lef1 into the scaffold protein E. coli thioredoxin A (Trx). All three classes of aptamers bound to Smads by GST pulldown assays and co-immunoprecipitation from mammalian cells. Expression of the aptamers in HepG2 cells did not generally inhibit Smad-dependent signaling as evaluated using seven TGF-beta responsive luciferase reporter genes. The Trx-xFoxH1b aptamer inhibited TGF-beta-induced expression from a reporter dependent on the Smad-FoxH1 interaction, A3-lux, by 50%. Trx-xFoxH1b also partially inhibited two reporters not dependent on a Smad-FoxH1 interaction, 3TP-lux and Twntop, and endogenous PAI-1 expression. Trx-Lef1 aptamer only inhibited expression of the Smad-Lef1 responsive reporter gene TwnTop. The Trx-CBP aptamer had no significant effect on reporter gene expression. The results suggest that Smad-binding peptide aptamers can be developed to selectively inhibit TGF-beta-induced gene expression.

Indexed as

Amino Acid SequenceAnimalsCarcinoma, HepatocellularCarrier ProteinsCell Line, TumorCorticosteroneDNA-Binding ProteinsForkhead Transcription FactorsGene Expression Regulation, NeoplasticGenes, ReporterGlutathione TransferaseHumansLiver NeoplasmsLymphoid Enhancer-Binding Factor 1Open Reading FramesPolymerase Chain ReactionCarrier ProteinsCorticosteroneDNA-Binding ProteinsForkhead Transcription FactorsFOXH1 protein, humanFoxh1 protein, mouseGlutathione TransferaseLEF1 protein, humanLymphoid Enhancer-Binding Factor 1Smad3 ProteinSMAD3 protein, humanTrans-ActivatorsTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID15750622
OpenAlexW2037795068

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.