Zebrafish Heart Development Is Regulated Via Glutaredoxin 2 Dependent Migration And Survival Of Neural Crest Cells. - Info and Reading Options
By Berndt, Carsten, Poschmann, Gereon, Stuhler, Kai, Holmgren, Arne and Brautigam, Lars
"Zebrafish Heart Development Is Regulated Via Glutaredoxin 2 Dependent Migration And Survival Of Neural Crest Cells." and the language of the book is English.
“Zebrafish Heart Development Is Regulated Via Glutaredoxin 2 Dependent Migration And Survival Of Neural Crest Cells.” Metadata:
- Title: ➤ Zebrafish Heart Development Is Regulated Via Glutaredoxin 2 Dependent Migration And Survival Of Neural Crest Cells.
- Authors: Berndt, CarstenPoschmann, GereonStuhler, KaiHolmgren, ArneBrautigam, Lars
- Language: English
Edition Identifiers:
- Internet Archive ID: pubmed-PMC4060141
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"Zebrafish Heart Development Is Regulated Via Glutaredoxin 2 Dependent Migration And Survival Of Neural Crest Cells." Description:
The Internet Archive:
This article is from <a href="//archive.org/search.php?query=journaltitle%3A%28Redox%20Biology%29" rel="ugc nofollow">Redox Biology</a>, <a href="//archive.org/search.php?query=journaltitle%3A%28Redox%20Biology%29%20AND%20volume%3A%282%29" rel="ugc nofollow">volume 2</a>.<h2>Abstract</h2>Glutaredoxin 2 is a vertebrate specific oxidoreductase of the thioredoxin family of proteins modulating the intracellular thiol pool. Thereby, glutaredoxin 2 is important for specific redox signaling and regulates embryonic development of brain and vasculature via reversible oxidative posttranslational thiol modifications. Here, we describe that glutaredoxin 2 is also required for successful heart formation. Knock-down of glutaredoxin 2 in zebrafish embryos inhibits the invasion of cardiac neural crest cells into the primary heart field. This leads to impaired heart looping and subsequent obstructed blood flow. Glutaredoxin 2 specificity of the observed phenotype was confirmed by rescue experiments. Active site variants of glutaredoxin 2 revealed that the (de)-glutathionylation activity is required for proper heart formation. Our data suggest that actin might be one target during glutaredoxin 2 regulated cardiac neural crest cell migration and embryonic heart development. In summary, this work represents further evidence for the general importance of redox signaling in embryonic development and highlights additionally the importance of glutaredoxin 2 during embryogenesis.
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