PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications

Protein kinase R (PKR) has been suggested to act as a mediator of ER stress and inflammation in obesity. Here, Lancaster et al. find that genetic loss of PKR does not alter the development of obesity, and suggest that the use of littermate controls may explain differences in mouse knockout phenotype...

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Autores principales: G. I. Lancaster, H. L. Kammoun, M. J. Kraakman, G. M. Kowalski, C. R. Bruce, M. A. Febbraio
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2016
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Acceso en línea:https://doaj.org/article/33a5a266327947a0a8bd5841e6f42498
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