ArticleMethods in molecular biology (Clifton, N.J.)2013
Identification of thioredoxin target protein networks in cardiac tissues of a transgenic mouse.
Article in Methods in molecular biology (Clifton, N.J.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Mitochondrial TrxR2 regulates metabolism and protects from metabolic disease through enhanced TCA and ETC function.Communications biology · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The advent of sensitive and robust quantitative proteomics techniques has been emerging as a vital tool for deciphering complex biological puzzles that would have been challenging to conventional molecular biology methods. The method here describes the use of two isotope labeling techniques-isobaric tags for relative and absolute quantification (iTRAQ) and redox isotope-coded affinity tags (ICAT)-to elucidate the cardiovascular redox-proteome changes and thioredoxin 1 (Trx1)-regulated protein network in cardiac-specific Trx1 transgenic mouse models. The strategy involves the use of an amine-labeling iTRAQ technique, gauging the global proteome changes in Trx1 transgenic mice at the protein level, while ICAT, labeling redox-sensitive cysteines, reveals the redox status of cysteine residues. Collectively, these two quantitative proteomics techniques can not only quantify global changes of the cardiovascular proteome but also pinpoint specific redox-sensitive cysteine sites that are subjected to Trx1-catalyzed reduction.
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