Evidence map›Paper›PMID 11359898›Full record

ArticleMolecular and cellular biology2001

Swift is a novel BRCT domain coactivator of Smad2 in transforming growth factor beta signaling.

K Shimizu, P Y Bourillot, S J Nielsen, A M Zorn, J B Gurdon

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

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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 at 3 institutions in 1 country.

K ShimizuWellcome Trust Cancer Research Campaign Institute, Cambridge CB2 1QR, United Kingdom.
P Y Bourillot
S J Nielsen
A M Zorn
J B Gurdon
University of Cambridge · GBWellcome/Cancer Research UK Gurdon Institute · GBWellcome Trust · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Transforming growth factor beta (TGFbeta) signaling is transduced via Smad2-Smad4-DNA-binding protein complexes which bind to responsive elements in the promoters of target genes. However, the mechanism of how the complexes activate the target genes is unclear. Here we identify Xenopus Swift, a novel nuclear BRCT (BRCA1 C-terminal) domain protein that physically interacts with Smad2 via its BRCT domains. We examine the activity of Swift in relation to gene activation in Xenopus embryos. Swift mRNA has an expression pattern similar to that of Smad2. Swift has intrinsic transactivation activity and activates target gene transcription in a TGFbeta-Smad2-dependent manner. Inhibition of Swift activity results in the suppression of TGFbeta-induced gene transcription and defective mesendoderm development. Blocking Swift function affects neither bone morphogenic protein nor fibroblast growth factor signaling during early development. We conclude that Swift is a novel coactivator of Smad2 and that Swift has a critical role in embryonic TGFbeta-induced gene transcription. Our results suggest that Swift may be a general component of TGFbeta signaling.

Indexed as

Xenopus ProteinsAmino Acid SequenceAnimalsBRCA1 ProteinCloning, MolecularDNA-Binding ProteinsGene Expression Regulation, DevelopmentalMolecular Sequence DataProtein Structure, TertiaryRNA, MessengerSequence Homology, Amino AcidSignal TransductionSmad2 ProteinTrans-ActivatorsTranscriptional ActivationTransforming Growth Factor betaBRCA1 ProteinDNA-Binding ProteinsPAXIP1 protein, XenopusRNA, MessengerSmad2 ProteinSmad2 protein, XenopusTrans-ActivatorsTransforming Growth Factor betaXenopus Proteins

Identifiers

PMID11359898
PMCPMC87053
OpenAlexW2126794028

What OpenQuestion holds

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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.