Evidence map›Paper›PMID 23221633›Full record

ArticleNucleic acids research2013

Novel Smad proteins localize to IR-induced double-strand breaks: interplay between TGFβ and ATM pathways.

Minli Wang, Janapriya Saha, Megumi Hada, Jennifer A Anderson, Janice M Pluth, Peter O'Neill, Francis A Cucinotta

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-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

26 citing papers in PubMed, 56 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

7 authors at 4 institutions in 2 countries.

Minli WangUSRA Division of Life Sciences, Houston, TX 77058, USA.
Janapriya Saha
Megumi Hada
Jennifer A Anderson
Janice M Pluth
Peter O'Neill
Francis A Cucinotta
Johnson Space Center · USLawrence Berkeley National Laboratory · USCRUK/MRC Oxford Institute for Radiation Oncology · GBNational Space Biomedical Research Institute · US

Funding

Medical Research Council MC_PC_12001
6 · The paper itself

Abstract

Cellular damage from ionizing radiation (IR) is in part due to DNA damage and reactive oxygen species, which activate DNA damage response (DDR) and cytokine signaling pathways, including the ataxia telangiectasia mutated (ATM) and transforming growth factor (TGF)β/Smad pathways. Using classic double-strand breaks (DSBs) markers, we studied the roles of Smad proteins in DDR and the crosstalk between TGFβ and ATM pathways. We observed co-localization of phospho-Smad2 (pSmad2) and Smad7 with DSB repair proteins following low and high linear energy transfer (LET) radiation in human fibroblasts and epithelial cells. The decays of both foci were similar to that of γH2AX foci. Irradiation with high LET particles induced pSmad2 and Smad7 foci tracks indicating the particle trajectory through cells. pSmad2 foci were absent in S phase cells, while Smad7 foci were present in all phases of cell cycle. pSmad2 (but not Smad7) foci were completely abolished when ATM was depleted or inactivated. In contrast, a TGFβ receptor 1 (TGFβR1) inhibitor abrogated Smad7, but not pSmad2 foci at DSBs sites. In summary, we suggest that Smad2 and Smad7 contribute to IR-induced DSB signaling in an ATM or TGFβR1-dependent manner, respectively.

Indexed as

DNA Breaks, Double-StrandedActivating Transcription Factor 2Ataxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineDNA-Binding ProteinsHistonesHumansKineticsLinear Energy TransferPhosphorylationProtein Serine-Threonine KinasesRadiation, IonizingSmad2 ProteinSmad3 ProteinSmad7 ProteinActivating Transcription Factor 2Ataxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsH2AX protein, humanHistonesProtein Serine-Threonine KinasesSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanSmad7 ProteinSMAD7 protein, humanTransforming Growth Factor betaTumor Suppressor Proteins

Identifiers

PMID23221633
PMCPMC3553971
OpenAlexW2075410218

What OpenQuestion holds

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LicenceCC BY-NC
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.