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...
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Nature Publishing Group
2016-02-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/ncomms10626 |