Evidence map›Paper›PMID 16775010›Full record

ArticleMolecular biology of the cell2006

Inhibition of transforming growth factor-beta1-induced signaling and epithelial-to-mesenchymal transition by the Smad-binding peptide aptamer Trx-SARA.

Bryan M Zhao, F Michael Hoffmann

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

42 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024
    Review
  3. Review
  4. Review
  5. TGFβ signaling pathways in human health and disease.Frontiers in molecular biosciences · 2023
    Review
  6. Article
  7. Review
  8. The Role of TGF-Evidence-based complementary and alternative medicine : eCAM · 2021
    Review
  9. Article
  10. Long Noncoding RNA TP73-AS1 Targets MicroRNA-329-3p to Regulate Expression of the SMAD2 Gene in Human Cervical Cancer Tissue and Cell Lines.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  11. Article
  12. Article
  13. Transforming growth factor-β: A therapeutic target for cancer.Human vaccines & immunotherapeutics · 2017
    Review
  14. Article
  15. Review
  16. Two faces of TGF-beta1 in breast cancer.Mediators of inflammation · 2014
    Review
  17. Article
  18. Targeting TGF-β signaling in cancer.Expert opinion on therapeutic targets · 2013
    Review
  19. Review
  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.

Bryan M ZhaoMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA.
F Michael Hoffmann
Center for Cancer Research · 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
NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA090875NCI NIH HHS T32 CA009135NCI NIH HHS T32-CA09135
6 · The paper itself

Abstract

Overexpression of the inhibitory Smad, Smad7, is used frequently to implicate the Smad pathway in cellular responses to transforming growth factor beta (TGF-beta) signaling; however, Smad7 regulates several other proteins, including Cdc42, p38MAPK, and beta-catenin. We report an alternative approach for more specifically disrupting Smad-dependent signaling using a peptide aptamer, Trx-SARA, which comprises a rigid scaffold, the Escherichia coli thioredoxin A protein (Trx), displaying a constrained 56-amino acid Smad-binding motif from the Smad anchor for receptor activation (SARA) protein. Trx-SARA bound specifically to Smad2 and Smad3 and inhibited both TGF-beta-induced reporter gene expression and epithelial-to-mesenchymal transition in NMuMG murine mammary epithelial cells. In contrast to Smad7, Trx-SARA had no effect on the Smad2 or 3 phosphorylation levels induced by TGF-beta1. Trx-SARA was primarily localized to the nucleus and perturbed the normal cytoplasmic localization of Smad2 and 3 to a nuclear localization in the absence of TGF-beta1, consistent with reduced Smad nuclear export. The key mode of action of Trx-SARA was to reduce the level of Smad2 and Smad3 in complex with Smad4 after TGF-beta1 stimulation, a mechanism of action consistent with the preferential binding of SARA to monomeric Smad protein and Trx-SARA-mediated disruption of active Smad complexes.

Indexed as

Amino Acid SequenceAnimalsAptamers, PeptideCell NucleusCells, CulturedCytoplasmEpithelial CellsExtracellular Signal-Regulated MAP KinasesHumansIntracellular Signaling Peptides and ProteinsMesodermMiceMolecular Sequence DataMultiprotein Complexesp38 Mitogen-Activated Protein KinasesPhosphorylationAptamers, PeptideExtracellular Signal-Regulated MAP KinasesIntracellular Signaling Peptides and ProteinsMultiprotein Complexesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktSerine EndopeptidasesSmad ProteinsTGFB1 protein, humanTgfb1 protein, mouseThioredoxinsTransforming Growth Factor betaTransforming Growth Factor beta1ZFYVE16 protein, human

Identifiers

PMID16775010
PMCPMC1556379
OpenAlexW2166289632

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.